Re: Fats & Cholesterol

[Guest guest]

Hi Katy,

> from any of my medical sources, from Nutrition experts. For months now

> I've been reading that Cholesterol is a response to weakened walls of blood

> vessels and does indeed repair them by overlaying the weakened spots.

I don't doubt that, but the reason none of the active atherosclerosis

researchers believe this is because all of the research contradicts

it. Lipid accumulation causes inflammation, connective tissue

buildup, and weakening of the fibrous caps. A much better " repair "

scenario would be multiplying the healthy cells!

Chris

[Guest guest]

> You can look at the original Burr and Burr study from 1929 if you

> want. The Journal of Biological Chemistry has their entire archives

> free online and you should be able to find it through an

> author/keyword search pretty quickly. For a more comprehensive

> review, my Special Report will hopefully be out soon, though it keeps

> getting delayed. Some of Ray Peat's writings are useful, though he

> doesn't always provide enough detail to make his case to a skeptic in

> my opinion.

Thanks, I look forward to reading up.

> Good point regarding intolerances. What are you able to eat?

Most vegetables if cooked well (have to be very careful with cruciferous,

nightshades &

fibrous leafy greens), eggs in abundance, raw milk, cheese & cream, soaked

grains, bread

made from freshly ground flour and soaked (as described in NT), some fruits,

fish, poultry,

occasional very small amounts of red meat, CLO, butter, coconut oil (both in

abundance).

K.

[Guest guest]

Of course the researchers have those findings, they are tied to big pharma and

want to sell more Lipitor or whatever....

Quite frankly I have as little respect for mst researchers as I have for

Doctors in general and oc the FDA, and their buddies in the drug industry.

Still Lipid accumulation is a result of an acid -deseased body- in it's attempts

t heal itself of the damage it produces cholesterol. Cholesterol is the effect

not the cause of our problems, it is much better to say Why is there so much

Cholesterol?

Katy

> from any of my medical sources, from Nutrition experts. For months now

> I've been reading that Cholesterol is a response to weakened walls of blood

> vessels and does indeed repair them by overlaying the weakened spots.

I don't doubt that, but the reason none of the active atherosclerosis

researchers believe this is because all of the research contradicts

it. Lipid accumulation causes inflammation, connective tissue

buildup, and weakening of the fibrous caps. A much better " repair "

scenario would be multiplying the healthy cells!

Chris

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9:13 AM

[Guest guest]

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

> I can't tolerate organ meats or red meats at all. I also have

> trouble tolerating dark, leafy green vegetables because of their

> fiber content.

K, red meats are often high in amines because they are " aged "

for flavor. I think I read that organ meats are often high in amines

as well, but I don't recall why. Dark leafy vegetables tend to be

high in salicylates. Just FYI.

[Guest guest]

Hi

> Most vegetables if cooked well (have to be very careful with cruciferous,

> nightshades &

> fibrous leafy greens), eggs in abundance, raw milk, cheese & cream, soaked

> grains, bread

> made from freshly ground flour and soaked (as described in NT), some fruits,

> fish, poultry,

> occasional very small amounts of red meat, CLO, butter, coconut oil (both in

> abundance).

It doesn't sound to me like you should need any supplemental oil with

PUFA. Eggs are rich in PUFA, butterfat has enough PUFA to meet the

requirement all by itself at 40% of calories, so at a lower amount

still supplies a substantial contribution, and you have small amounts

of PUFA in the other foods that add up. However, if you have signs of

deficiency that resolve with an added oil, I can't really argue with

that. But in the absence of any kind of dermatitis or dry skin that

does so, I would not personally bother.

Chris

[Guest guest]

Katy,

> Of course the researchers have those findings, they are tied to big pharma

> and want to sell more Lipitor or whatever....

First, not all lipid researchers are working for Big Pharma.

Espcially in nutrition research groups, most researchers seem to be

very whole foods-oriented nutrition-as-medicine type people. Even the

ones who are working with Big Pharma have to deal with real data.

Fraud is an issue, but by an large I think real data is just

manipulated to exaggerate benefits of drugs or emphasized in the wrong

way or interpreted the wrong way rather than outright fraudulent.

> Quite frankly I have as little respect for mst researchers as I have for

> Doctors in general and oc the FDA, and their buddies in the drug industry.

> Still Lipid accumulation is a result of an acid -deseased body- in it's

> attempts t heal itself of the damage it produces cholesterol. Cholesterol

> is the effect not the cause of our problems, it is much better to say Why is

> there so much Cholesterol?

I'm not interested in blaming the disease on cholesterol, but there is

a fundamental problem with your theory, which is that accumulation of

cholesterol in macrophages causes a worsening of the disease process.

It does not fix anything.

The question of why there is so much cholesterol is, of course

interesting, but the amount of cholesterol is not what contributes to

the disease. What contributes to the disease is the oxidation and

glycation of LDL (and the numerous other things I listed in the " heart

attack " thread, and possibly other ones), and the oxidation is

stimulated by high PUFA in the LDL membrane and low antioxidant

levels. If anything, the cholesterol is protective, because the large

LDL particles that have more cholesterol in them are less likely to

oxidize.

Chris

[Guest guest]

consider for the moment the 'fact' that we tend to repeat- and reiterate

our prejudices, rare is the open-mind, rarer is the researcher [steeped in the

knowledge pounded into him by schools that insist they [parrot 'known facts']no

matter what his allegiance who won't spout the party-line until the truth smacks

him/her in the face. I still contend cholesterol is a vessel repairer gone

crazy in a sick body.

Katy,

> Of course the researchers have those findings, they are tied to big pharma

> and want to sell more Lipitor or whatever....

First, not all lipid researchers are working for Big Pharma.

Espcially in nutrition research groups, most researchers seem to be

very whole foods-oriented nutrition-as-medicine type people. Even the

ones who are working with Big Pharma have to deal with real data.

Fraud is an issue, but by an large I think real data is just

manipulated to exaggerate benefits of drugs or emphasized in the wrong

way or interpreted the wrong way rather than outright fraudulent.

> Quite frankly I have as little respect for mst researchers as I have for

> Doctors in general and oc the FDA, and their buddies in the drug industry.

> Still Lipid accumulation is a result of an acid -deseased body- in it's

> attempts t heal itself of the damage it produces cholesterol. Cholesterol

> is the effect not the cause of our problems, it is much better to say Why is

> there so much Cholesterol?

I'm not interested in blaming the disease on cholesterol, but there is

a fundamental problem with your theory, which is that accumulation of

cholesterol in macrophages causes a worsening of the disease process.

It does not fix anything.

The question of why there is so much cholesterol is, of course

interesting, but the amount of cholesterol is not what contributes to

the disease. What contributes to the disease is the oxidation and

glycation of LDL (and the numerous other things I listed in the " heart

attack " thread, and possibly other ones), and the oxidation is

stimulated by high PUFA in the LDL membrane and low antioxidant

levels. If anything, the cholesterol is protective, because the large

LDL particles that have more cholesterol in them are less likely to

oxidize.

Chris

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9:13 AM

[Guest guest]

Hi Katy,

> consider for the moment the 'fact' that we tend to repeat- and

> reiterate our prejudices, rare is the open-mind, rarer is the researcher

> [steeped in the knowledge pounded into him by schools that insist they

> [parrot 'known facts']no matter what his allegiance who won't spout the

> party-line until the truth smacks him/her in the face.

Well I hardly think this characterizes me. Certainly I have my faults

and have to struggle daily to be open-minded and humble and charitable

to alternative ideas, but I have lots of ideas that are very contrary

to what is generally accepted -- for example, my opinions on PUFA I've

recently been sharing, or on the cooperative nature of vitamins A and

D I've written about -- and I usually go out of my way to admit I'm

wrong about something if I discover that's the case.

I believed in the " atherosclerosis is protective " idea when I first

read it in Uffe Ravnskov's book. But, if I were like you criticize, I

would accept this idea simply because I've been steeped in the WAPF

and Ravnskov is associated therewith and promoted thereby, and thus I

would stick with believing it. On the contrary, I think doing a

greater deal of reading, including the peer-reviewed research and

including books on both sides of the argument, such as Ravnskov's,

Colpo's, (these two are anti-lipid hypothesis) and Steinberg's (this

one is pro-lipid hypothesis), has led me to consider this idea simply

wrong.

> I still contend cholesterol is a vessel repairer gone crazy in a sick body.

We can each contend all we want, but ultimately it comes down to

evidence. The simple fact of the matter is that cholesterol

accumulating in macrophages activates the inflammatory process that

leads to further development of atherosclerosis, rather than

forestalling that process or reversing it.

The idea that plaque buildup is repairing the vessel wall is also

difficult to reconcile with the fact that LDL has to oxidize in order

to get cholesterol into the vessel wall. If the cholesterol getting

into the wall is a *good* thing, why does it require a pathologic

process to happen? I'm referring here not to a pathologic process in

the vessel wall, but to a pathologic process in the lipoprotein. The

putative " repair substance " should not have to get damaged in order to

do the repairing.

If the accumulation of lipid in the vessel wall is good, then we

should eat a diet high in refined vegetable oils, because these will

increase oxidation of LDL and allow us to place more " protective "

lipid into the vessel wall.

Chris

[Guest guest]

> We can each contend all we want, but ultimately it comes down to

> evidence. The simple fact of the matter is that cholesterol

> accumulating in macrophages activates the inflammatory process that

> leads to further development of atherosclerosis, rather than

> forestalling that process or reversing it.

>

> The idea that plaque buildup is repairing the vessel wall is also

> difficult to reconcile with the fact that LDL has to oxidize in order

> to get cholesterol into the vessel wall. If the cholesterol getting

> into the wall is a *good* thing, why does it require a pathologic

> process to happen? I'm referring here not to a pathologic process in

> the vessel wall, but to a pathologic process in the lipoprotein. The

> putative " repair substance " should not have to get damaged in order to

> do the repairing.

>

> If the accumulation of lipid in the vessel wall is good, then we

> should eat a diet high in refined vegetable oils, because these will

> increase oxidation of LDL and allow us to place more " protective "

> lipid into the vessel wall.

>

> Chris

I have to say your explanation makes a lot of sense. However, I have not yet

read the

Steinberg book and thus have not seen the evidence you have. The majority of

the

evidence I've seen contradicts the lipid hypothesis (Ravnskov, Enig, Colpo,

Kendrick, etc.).

I would love to take a look at the evidence that changed your mind. Was it in

the

Steinberg book? I checked out the Peat articles, and was underwhelmed.

One question I have about the theory that oxidized LDL is a primary cause of CHD

(without

other intervening factors unrelated to ox-LDL) is that fact that statins have

been

demonstrated to lower concentrations of ox-LDL - but they do not lower rates of

CHD in

women, the elderly or primary prevention population. What do you believe

explains this

discrepancy?

K.

[Guest guest]

no, it was no criticism of you, I tried hard to keep you from taking it

that way, I was thinking of a lecture /I heard this morning re: how our thinking

affects our judgments and conclusions, He [Dr. R. DiCenso speaking of

Whole-person therapy]-said that before the age of 7 we are told what to do, how

to think, even how we should feel about different things, so when at 7 we begin

to start thinking for ourselves we do so using the prejudices and conclusions

we've already been taught, If I thought you were closed-minded I wouldn't be

here, many 'Natural' Docs say they came out of med school believing the whole

patter complete, but as they learned more their conclusions changed, I have been

listening to a series of lectures by Alternative thinking Doctors and nearly all

of the talks began thus.

I think when it comes to research much of the results are interpreted with the

cholesterol theory as the basis, just as; oh dare I say it, ok, just as the

Theories of evolution have been perpetuated.

I apologize that I caused you think I have been tossing you in the 'spoiled'

basket.

> consider for the moment the 'fact' that we tend to repeat- and

> reiterate our prejudices, rare is the open-mind, rarer is the researcher

> [steeped in the knowledge pounded into him by schools that insist they

> [parrot 'known facts']no matter what his allegiance who won't spout the

> party-line until the truth smacks him/her in the face.

Well I hardly think this characterizes me. Certainly I have my faults

and have to struggle daily to be open-minded and humble and charitable

to alternative ideas, but I have lots of ideas that are very contrary

to what is generally accepted -- for example, my opinions on PUFA I've

recently been sharing, or on the cooperative nature of vitamins A and

D I've written about -- and I usually go out of my way to admit I'm

wrong about something if I discover that's the case.

I believed in the " atherosclerosis is protective " idea when I first

read it in Uffe Ravnskov's book. But, if I were like you criticize, I

would accept this idea simply because I've been steeped in the WAPF

and Ravnskov is associated therewith and promoted thereby, and thus I

would stick with believing it. On the contrary, I think doing a

greater deal of reading, including the peer-reviewed research and

including books on both sides of the argument, such as Ravnskov's,

Colpo's, (these two are anti-lipid hypothesis) and Steinberg's (this

one is pro-lipid hypothesis), has led me to consid

> I still contend cholesterol is a vessel repairer gone crazy in a sick body.

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[Guest guest]

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

That gives you a little over 3,000 IU per day. I would consider

boosting it to see if it helps.

looking at the bottle, I'm getting a total off 11,250IU of Vit

A/ day from the CLO. Is that adequate? From the way I ate prior to

last summer, I'm probably deficient in about everything imaginable, lol.

Also, the chicken is local and free range. They get a little bit of

grain supplement (not organic) but it's the best compromise financially

between organic and grocery store.

[Guest guest]

On 2/7/08, chriskjezp <chriskresser@...> wrote:

> I would love to take a look at the evidence that changed your mind. Was it

> in the

> Steinberg book? I checked out the Peat articles, and was underwhelmed.

The Steinberg book is good, but has its faults. Here is my review:

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

However, on the specific issue of whether atherosclerotic plaque is

good for you or not (Ravnskov essentially says that the plaque not

containing complex lesions is good for you and is protecting blood

vessles in certain areas exposed to high pressure), there is a 2002

review by Libby on the relationship of inflammation to atherosclerosis

(you can find this on pubmed) that presented contrary evidence.

Also, my research into nitric oxide provides a better explanation for

why atherosclerotic plaque occurs in areas exposed to perpindicular

blood flow -- because this reduces shear stress, which is the main

stimulator of nitric oxide synthase expression.

So, rather then plaque reinforcing the vessel wall to deal with this

pressure, the plaque occurs because the pressure is inhibiting nitric

oxide, and thus eliminating the primary defense against

atherosclerosis. Nitric oxide prevents LDL oxidation, and oxidized

LDL further diminishes nitric oxide production. Nitric oxide's most

important effects are increasing vessel dilation, decreasing adhesion

of white blood cells and migration of smooth muscle cells and

inhibiting clot formation.

And thinking about it, producing atherosclerotic plaque is probably

not the best way of reinforcing the vessel wall. And exercise

increases the pressure experienced, yet decreases atherosclerosis.

This is probably because exercise increases shear stress through

parallel blood flow, upregulating nitric oxide production.

Finally, Steinberg does a pretty good job showing that the

cholesterol-fed rabbit *is* relevant to human atherosclerosis and is

essentially the same thing, and it seems pretty clear from the

research discussed in his book that fatty streaks and regular

atherosclerosis are in fact early stages of complex lesion

atherosclerosis. Ravnskov asserts that they essentially have nothing

to do with each other, which is difficult to reconcile to the fact

that they occur progressively in the cholesterol-fed rabbit model.

> One question I have about the theory that oxidized LDL is a primary cause of

> CHD (without

> other intervening factors unrelated to ox-LDL)

Well I am not saying it is the *primary* cause of atherosclerosis. It

is very difficult to tease out its contribution to the contribution of

Rho Acitvation:

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

> is that fact that statins

> have been

> demonstrated to lower concentrations of ox-LDL - but they do not lower rates

> of CHD in

> women, the elderly or primary prevention population. What do you believe

> explains this

> discrepancy?

I'm not sure that discrepancy actually exists. I have read both ways

on whether they are protective in these populations, and also read

that it is very understudied. Do you have a reference for this? I

realize I am saying things without providing all the references but

since there is conflicting information on this point I can't really

address it without seeing the data.

Chris

[Guest guest]

,

I know allergies are usually to proteins but you can become allergic to

just about anything. I know beyond any doubt it's the Iodine I'm

allergic to. I had mild reactions to a few medical tests over the

years, then in 1997, they did a cardiac cath (the dye is iodine based)

and I had an all out anaphylactic reaction even though I was pretreated

for 24 hours with IV steroids and Benadryl. I am severely hypothyroid

and have tried to supplement with Iodine, but I immediately get throat

itching and swelling tight chest etc. I've tried spirulina and kelp

with the same reaction. I can tolerate tiny amounts, like what's in

sea salt, but not anything with significant amounts of Iodine. I too

don't understand how you can be so allergic to an " essential "

nutrient. I've asked this in other groups, but nobody has come up with

an answer, lol.

Patty

Is it perhaps a protein that has iodine in it that causes these

allergies?

>

>

>

[Guest guest]

Hi Katy,

> no, it was no criticism of you, I tried hard to keep you from taking

> it that way, I was thinking of a lecture /I heard this morning re: how our

> thinking affects our judgments and conclusions, He [Dr. R. DiCenso speaking

> of Whole-person therapy]-said that before the age of 7 we are told what to

> do, how to think, even how we should feel about different things, so when at

> 7 we begin to start thinking for ourselves we do so using the prejudices and

> conclusions we've already been taught, If I thought you were closed-minded I

> wouldn't be here, many 'Natural' Docs say they came out of med school

> believing the whole patter complete, but as they learned more their

> conclusions changed, I have been listening to a series of lectures by

> Alternative thinking Doctors and nearly all of the talks began thus.

> I think when it comes to research much of the results are interpreted with

> the cholesterol theory as the basis, just as; oh dare I say it, ok, just as

> the Theories of evolution have been perpetuated.

There is some truth to this but the grand difference between

atherosclerosis research and evolutionary research is that

atherosclerosis research is highly testable, whereas many things about

evolution are not. So, you can, for example, incubate an isolated

macrophage with oxidized LDL and see how it changes when it takes up

the LDL and the types of molecules it secretes and so on, and you can

do other research in the whole organism, and you can look at the issue

from many angles. Naturally, the types of questions you ask will bias

how you interpret the theory, but as to the specific question of

whether the cholesterol getting into the macrophages and into the

vessel wall is a good thing or not, it appears not.

Chris

[Guest guest]

Ah, We all have seen that in research one starts with an idea and tests

for it.

I believe our bodies were designed to heal themselves. But we are not designed

to live in the chemical soup we find ourselves in or to eat processed, GM foods,

I go back to my original conclusion, we need to look for Why the cholesterol has

begun to close the blood vessels. My grandparents ate huge quantities of whole

milk, butter, Lard, and other proscribed things for good cholesterol levels.

Katy

> no, it was no criticism of you, I tried hard to keep you from taking

> it that way, I was thinking of a lecture /I heard this morning re: how our

> thinking affects our judgments and conclusions, He [Dr. R. DiCenso speaking

> of Whole-person therapy]-said that before the age of 7 we are told what to

> do, how to think, even how we should feel about different things, so when at

> 7 we begin to start thinking for ourselves we do so using the prejudices and

> conclusions we've already been taught, If I thought you were closed-minded I

> wouldn't be here, many 'Natural' Docs say they came out of med school

> believing the whole patter complete, but as they learned more their

> conclusions changed, I have been listening to a series of lectures by

> Alternative thinking Doctors and nearly all of the talks began thus.

> I think when it comes to research much of the results are interpreted with

> the cholesterol theory as the basis, just as; oh dare I say it, ok, just as

> the Theories of evolution have been perpetuated.

There is some truth to this but the grand difference between

atherosclerosis research and evolutionary research is that

atherosclerosis research is highly testable, whereas many things about

evolution are not. So, you can, for example, incubate an isolated

macrophage with oxidized LDL and see how it changes when it takes up

the LDL and the types of molecules it secretes and so on, and you can

do other research in the whole organism, and you can look at the issue

from many angles. Naturally, the types of questions you ask will bias

how you interpret the theory, but as to the specific question of

whether the cholesterol getting into the macrophages and into the

vessel wall is a good thing or not, it appears not.

Chris

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9:13 AM

[Guest guest]

If you are asking me, or even if you aren't; I got mine from Dr. R, DiCenso and

Al G MSc BSc , are the latest to my collection of many people I've got

this same information from.

Katy

On 2/7/08, chriskjezp <chriskresser@...> wrote:

> I would love to take a look at the evidence that changed your mind. Was it

> in the

> Steinberg book? I checked out the Peat articles, and was underwhelmed.

The Steinberg book is good, but has its faults. Here is my review:

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

However, on the specific issue of whether atherosclerotic plaque is

good for you or not (Ravnskov essentially says that the plaque not

containing complex lesions is good for you and is protecting blood

vessles in certain areas exposed to high pressure), there is a 2002

review by Libby on the relationship of inflammation to atherosclerosis

(you can find this on pubmed) that presented contrary evidence.

Also, my research into nitric oxide provides a better explanation for

why atherosclerotic plaque occurs in areas exposed to perpindicular

blood flow -- because this reduces shear stress, which is the main

stimulator of nitric oxide synthase expression.

So, rather then plaque reinforcing the vessel wall to deal with this

pressure, the plaque occurs because the pressure is inhibiting nitric

oxide, and thus eliminating the primary defense against

atherosclerosis. Nitric oxide prevents LDL oxidation, and oxidized

LDL further diminishes nitric oxide production. Nitric oxide's most

important effects are increasing vessel dilation, decreasing adhesion

of white blood cells and migration of smooth muscle cells and

inhibiting clot formation.

And thinking about it, producing atherosclerotic plaque is probably

not the best way of reinforcing the vessel wall. And exercise

increases the pressure experienced, yet decreases atherosclerosis.

This is probably because exercise increases shear stress through

parallel blood flow, upregulating nitric oxide production.

Finally, Steinberg does a pretty good job showing that the

cholesterol-fed rabbit *is* relevant to human atherosclerosis and is

essentially the same thing, and it seems pretty clear from the

research discussed in his book that fatty streaks and regular

atherosclerosis are in fact early stages of complex lesion

atherosclerosis. Ravnskov asserts that they essentially have nothing

to do with each other, which is difficult to reconcile to the fact

that they occur progressively in the cholesterol-fed rabbit model.

> One question I have about the theory that oxidized LDL is a primary cause of

> CHD (without

> other intervening factors unrelated to ox-LDL)

Well I am not saying it is the *primary* cause of atherosclerosis. It

is very difficult to tease out its contribution to the contribution of

Rho Acitvation:

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

> is that fact that statins

> have been

> demonstrated to lower concentrations of ox-LDL - but they do not lower rates

> of CHD in

> women, the elderly or primary prevention population. What do you believe

> explains this

> discrepancy?

I'm not sure that discrepancy actually exists. I have read both ways

on whether they are protective in these populations, and also read

that it is very understudied. Do you have a reference for this? I

realize I am saying things without providing all the references but

since there is conflicting information on this point I can't really

address it without seeing the data.

Chris

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

No virus found in this incoming message.

Checked by AVG Free Edition.

Version: 7.5.516 / Virus Database: 269.19.20/1262 - Release Date: 2/6/2008

9:13 AM