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 About lp(a) 
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Post About lp(a)
If lp(a) is a form of LDL cholesterol, when you have a cholesterol test does it register in the LDL figure?

If you have high LDL does that mean you have high lp(a) - and vice versa?

I read somewhere, in the Track Your Plaque book, I think, that 17% of heart attack patients have high lp(a). That doesn't sound like a high figure, I would have expected it to be higher than that. Perhaps the PT works best for those people and others would not get so much benefit from it?

If you take VC alone, without lysine, will it eventually do the same job, reverse your atherosclerosis? I'm assuming that it will, because you are needing to give your body orthomolecular substances which it can use for repair & also detoxification in the case of VC, so it would work, but not as quickly as the full PT. Of course, there isn't any reason not to take lysine.

Basically I wondered how similar lp(a) is to LDL and whether the mechanisms by which VC cleans arteries with cholesterol will also clean arteries with lp(a) in them.


Fri Jun 10, 2011 12:58 am
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Ascorbate Wizard
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Post Re: About lp(a)
Great questions. Lets take them one by one.

Lone Dog wrote:
If lp(a) is a form of LDL cholesterol, when you have a cholesterol test does it register in the LDL figure?


Yes it would. (I know of know way to "screen" out the Lp(a) fraction.)

Quote:

If you have high LDL does that mean you have high lp(a) - and vice versa?


No, not necessarily.

Quote:
I read somewhere, in the Track Your Plaque book, I think, that 17% of heart attack patients have high lp(a). That doesn't sound like a high figure, I would have expected it to be higher than that. Perhaps the PT works best for those people and others would not get so much benefit from it?


What is this books' reference for the 17% number? Looks like a misprint. I remember that an Oxford study published in Circulation in the late 90s cited a figure from a meta analysis more like 71%.

This was our report after that study made news in 2000:


Quote:
Oxford meta-analysis of 27 large studies (09/04/2000) shows that people with high Lp(a) are 70% more likely to have a heart attack or stroke.


Quote:
If you take VC alone, without lysine, will it eventually do the same job, reverse your therosclerosis? I'm assuming that it will, because you are needing to give your body orthomolecular substances which it can use for repair & also detoxification in the case of VC, so it would work, but not as quickly as the full PT. Of course, there isn't any reason not to take lysine.


Lysine is essential and according to Pauling on the video UNIFIED THEORY lecture, we must get at least 1 g daily in our food to remain in "nitrogen balance." So it is literally impossible to take vitamin C without getting at least a little lysine.

Quote:
Basically I wondered how similar lp(a) is to LDL and whether the mechanisms by which VC cleans arteries with cholesterol will also clean arteries with lp(a) in them.



Lp(a) is an ordinary LDL particle with a "sticky" apo(a) particle attached to the surface. (The apo(a) is what contains the so-called lysine binding sites.)

The mechanism by which vitamin C/lysine "cleans" arteries is the method to clean Lp(a)/apo(a).

In fact, there is a Pauling/Rath U. S. patent to use vitamin C/lysine solutions prior to transplants to "clean" arteries of plaque 5,230,996 - http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&p=1&u=%2Fnetahtml%2FPTO%2Fsearch-bool.html&r=3&f=G&l=50&co1=AND&d=PTXT&s1=Pauling-$&s2=Rath-$&OS=Pauling-$+AND+Rath-$&RS=Pauling-$+AND+Rath-$

The "hidden" knowledge is that only Lp(a) - and not LDL alone - sticks to lysine.

The nobel prize winning knowledge of the lysine binding sites are not mentioned these days. Apparently, the medical knowledge "gatekeepers" realized that the lysine binding sites are only on Lp(a) - not ordinary LDL. Plaques stick to lysine residues (and perhaps proline) that appear after a crack in the artery. This is exposed collagen.

Only Lp(a) sticks (and thus forms plaques) and when this was discovered by Beisegal in Germany examining aortas post mortem, See: reference #2 http://internetwks.com/pauling/refs.html (this news brought to Pauling by Matthias Rath) Pauling began to advance his theory and therapy.

Summary: Only Lp(a) forms plaques not ordinary LDL.



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Fri Jun 10, 2011 9:05 am
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Post Re: About lp(a)
Thank you, Owen, I appreciate your help with these questions.

With regard to the type of cholesterol involved in plaque formation, is there any corroboration for Dr Rath that it is lp(a) rather than LDL?

I'm wondering if we could put lysine aside for the moment, and consider what degree of reversal of atherosclerosis is possible using VC alone? Also, I believe the Shutes had results using vitamin E, and Lester Morrison with chondroitin sulfate. All without lysine.

If lysine is the key, however, and lp(a) is found in plaque, it comes as a surprise that the PT doesn't work for some people, as surely if they took the recommended 6g of lysine per day that should take care of it.


Sat Jun 11, 2011 12:51 am
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Ascorbate Wizard
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Post Re: About lp(a)
Lone Dog wrote:
Thank you, Owen, I appreciate your help with these questions.

With regard to the type of cholesterol involved in plaque formation, is there any corroboration for Dr Rath that it is lp(a) rather than LDL?

Did you read/look at the Biesegal reference? Rath was on that team that made the discovery that it was only Lp(a) that formed plaques. (Really apo(a) - but this sticky particle is what makes an LDL an Lp(a).)

And again, this apo(a) is the only possible way. There are no "lysine binding site" on ordinary LDL - it is not sticky. (Per Levy's book and Unified Theory, LDL and other "material" (e.g. calcium) can accumulate in plaques in later stages of the process (as it must be the apo(a) in the plaque can then attach to LDL particles, probably via a proline binding site, but that is another story...)

Pauling/Rath's guinea pig experiments showed that at least in this animal, Lp(a) blood levels rise when vitamin C intake is reduced. This result led to their theory that Lp(a) acts as a surrogate for vitamin C.


Quote:
I'm wondering if we could put lysine aside for the moment, and consider what degree of reversal of atherosclerosis is possible using VC alone? Also, I believe the Shutes had results using vitamin E, and Lester Morrison with chondroitin sulfate. All without lysine.


Again, you may have missed my point that you cannot put aside lysine. It is essential and we all most get at least 1 gram daily to exist.

Vitamin E spares/recycles vitamin C.

Per Levy book, Chondritin Sulfate has the property (like Lp(a)) that it can shore up and stabilize weak arterial walls. (And again, because some vitamin C and lysine must be in the diet, vitamin E or Chrondroitin will never work completely alone.)

But the very first case report that Pauling wrote and articulates on the video lecture answers your question directly. Vitamin C by itself will not provide the immediate relief of symptoms that can be obtained by adding and equivalent high dosage of lysine. Here is the transcript of Pauling describing the very first time high lysine was tried, after vitamin C by itself didn't relieve symptoms. (from the heart disease video):


Quote:

Two and one half years ago, (1991) I was in a meeting of the National Academy of Sciences of the United States. I wa s in the hallway of the academy building and another member of the academy came up to me. He said, Dr. Pauling, " I have heart disease. My brother, my father both died of heart attacks. I am a biochemist but I was retired from the National Institutes of Health several years ago for disability because of my heart. I have had 3 by-pass operations, and I can't have any more by-pass operations. I like to walk, but I have trouble. After I have walked a little way I develop angina pectoris pain in my heart. If I take a nitroglycerin tablet, I can walk a little farther, and then I may have to take another nitroglycerin tablet." He went on to say," I have been taking vitamin C, 5 grams a day for several years because of your recommendation. Is there something else that I could do that would permit me to walk?"

I said, "I could make a suggestion, it has never been tried before. Take Lysine."

Well I didn't need to tell him what Lysine was, that it's an essential amino acid and you have to get around a gram a day to be in good health, and you get it in your foods, because he is one of the most distinguished biochemists in the United States, recipient of the National Medal of Science in the United States. So he said, how much shall I take? I thought, what do I know. I know that people get a gram or two in their food depending upon how much meat and fish they eat, that it's essential they have to get around one gram. It hasn't any known toxicity in animals or human beings. I said 5 grams, 5 grams a day. He thanked me.

A couple of months later he telephoned me and said its almost miraculous. I started taking a gram a day and 2 grams and so on. Within a month after I had reached 5 grams a day of Lysine in addition to my 5 grams of vitamin C, I could walk 2 miles without any nitroglycerin tablets or without any pain in the chest. He said he had cut down the amount of heart medicine he was taking in half. "It's almost miraculous," he said.

Another couple of months went by and he telephoned me and said that, "I was feeling so good the other day that I cut down a big tree in our yard, and was chopping it up for wood, and I was also painting the house, and I got chest pains", despite his 5 grams of lysine, so he said that he "went up to 6 grams of lysine and 6 grams of vitamin C and told me now "I am continuing chopping down, chopping up the tree and painting the house". And now a couple of years later he is still in fine health. [From the 1993 Linus Pauling Video on Heart Disease]



Quote:
If lysine is the key, however, and lp(a) is found in plaque, it comes as a surprise that the PT doesn't work for some people, as surely if they took the recommended 6g of lysine per day that should take care of it.


You are correct that it is surprising, at least until you read Dr. Levy's STOP AMERICA'S #1 KILLER - and you realize that long-standing "involved" plaques are more like tissue - callouses - than plaster casts that can be dissolved by lysine.

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Sat Jun 11, 2011 9:14 am
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Post Re: About lp(a)
Lone Dog wrote:
If lp(a) is a form of LDL cholesterol, when you have a cholesterol test does it register in the LDL figure?
LDL, HDL, and cholesterol are different and exclusive categories. LDL cholesterol is an oxymoron (in the way you seem to be using the term). LDL and HDL are like containers. The cholesterol particles are what those containers carry around the body. The following interview of Ph.D. candidate Chris Masterjohn is an excellent primer for beginners about all of this (although they don't mention vitamin C very much).

The Healthy Skeptic Podcast – Episode 11, webpage with summary and download link

Direct download link to Episode 11 podcast file (MP3)(41.3 MB)

Quote:
In this episode, we discuss (among other things):
* the history of the cholesterol-heart disease connection
* misconceptions around diet vs. lipid hypothesis
* finding middle ground between cholesterol skeptics and proponents of the lipid hypothesis
* the LDL receptor and familial hypercholesterolemia and what they can tell us about cholesterol and Chronic Heart Disease in normal populations


Sat Jun 11, 2011 1:13 pm
Post Re: About lp(a)
Here are parts of three excellent responses by Chris Masterjohn to questions in the Comments section of the webpage that links to the episode 11 podcast:
Quote:
...LDL particle size can very easily be seen as a marker for time spent in the blood (because this leads to loss of triglycerides to cells and to HDL, and acquisition of cholesterol from HDL, more oxidation and other modifications, all of which make LDL small and dense). Since excess time spent in the blood is primarily a function of poor LDL receptor activity, and since poor LDL receptor activity is by far and away the most definitively established causal risk factor for heart disease, it makes sense to first and foremost consider small dense LDL as a risk factor because it is a marker for poor LDL receptor activity and long time spent in the blood. Thus, there is no reason to assume that treatments that boost LDL particle size through any means other than promoting better LDL receptor activity or preventing oxidation will actually prevent heart disease.
- Chris Masterjohn, June 9, 2011 at 10:09 pm

Quote:
...the LDL particle is a cargo ship. It is supposed to land at various docks to deliver over the goods. However, it is also supposed to protect the goods so that they are in good shape when the ship gets to the dock. However, there are often pirates at sea, and they may attack both the people at shore as well as the cargo ships. If they block entry to the dock, the ship cannot refuel or purchase more ammunition for defense. If the ship is thus left at sea, it runs out of ammunition and the pirates are then able to effectively sabotage it, ruin its goods, and purposefully plant explosives and release infectious diseases on the boat. Then, when it does get near shoreline, the folks at the dock catch illnesses and are caught in terrorist explosions. Thus, the immune system, like a navy and national guard, rescues the cargo ships that have been attacked (oxidized LDL), and quarantines them and any toxic factors released from them in something like a superfund site, where the surrounding community is protected as best as possible.
- Chris Masterjohn, June 10, 2011 at 4:10 pm

Quote:
...the localization of plaques is clearly related to hemodynamic factors. In any species, to my knowledge, including humans and rabbits, plaques occur in areas of disturbed blood flow. Shear stress, caused by uninterrupted parallel blood flow, increases synthesis of nitric oxide which is a protective factor in the optimal range, and, probably more importantly, upregulates tight junction proteins which decrease the permeability of the vessel. It has been experimentally demonstrated for near 100 years that plaques occur where the blood vessels are most permeable, and that anything affecting the permeability causes a proportional affect in the degree of atherosclerosis. Inflammation, for example, causes a general increase in permeability and thus enhances atherosclerosis. Exercise should theoretically have the opposite effect, since it increases blood flow and thus shear stress.
- Chris Masterjohn, June 11, 2011 at 1:02 pm
http://thehealthyskeptic.org/the-healthy-skeptic-podcast-episode-11


Sat Jun 11, 2011 2:00 pm
Ascorbate Wizard
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Post Re: About lp(a)
Quote:
LDL, HDL, and cholesterol are different and exclusive categories.

Huh? Are you sure you don't want to revise and extend your remarks? ( LDL and HDL are cholesterol.) But his question (which you didn't address) is whether Lp(a) is included in the LDL number on cholesterol tests. The answer is yes.

As far as what you hilighted, I hope you have quoted this fellow Chris Masterjohn out of context as
Quote:
and since poor LDL receptor activity is by far and away the most definitively established causal risk factor for heart disease,


is outlandish. LDL receptor for what? Who has definitely established it, what ever it is, as "far and away" a causal risk factor for heart disease?

And why is this posted in a thread devoted to Lp(a)?

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Sat Jun 11, 2011 2:41 pm
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Post Re: About lp(a)
ofonorow wrote:
Huh? Are you sure you don't want to revise and extend your remarks? ( LDL and HDL are cholesterol.)
Once again you would not deign to glance at the materials I'm referencing. Seems you haven't read any of Cutler's work, and now deja vu all over again with this Masterjohn interview... :roll:

ofonorow wrote:
But his question (which you didn't address) is whether Lp(a) is included in the LDL number on cholesterol tests. The answer is yes.
I have no reason to doubt you are correct in saying that. I saw no need for me to address it since you already had. No need to get you panties in a twist, Owen, if someone clarifies an important side-issue (in this case, the meaning of the word 'cholesterol'?) and doesn't talk about the main issue {in this case, Lp(a)}.

ofonorow wrote:
As far as what you hilighted, I hope you have quoted this fellow Chris Masterjohn out of context...
Nope. That's what he wrote alright.

ofonorow wrote:
...I hope you have quoted this fellow Chris Masterjohn out of context as
Quote:
and since poor LDL receptor activity is by far and away the most definitively established causal risk factor for heart disease,
is outlandish.
Time will tell Owen. Time will only tell.
ofonorow wrote:
LDL receptor for what? Who has definitely established it, what ever it is, as "far and away" a causal risk factor for heart disease?
Don't know yet. But I'm learning.
Isn't this something a professional naturopath should know something about?

ofonorow wrote:
And why is this posted in a thread devoted to Lp(a)?

Because LDL cholesterol is an oxymoron in the way it was being used. Better to nip these basic misunderstandings in the bud, no?


Sat Jun 11, 2011 6:13 pm
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Post Re: About lp(a)
Owen, has the lp(a) in plaque idea been confirmed by any other studies? I know Dr Rath was part of the team in the reference, but has their finding been confirmed by others?

Yes, I know what you are saying re: lysine. But others have had results without it, I'm not saying we shouldn't take it, however. The 'Track Your Plaque' program seems to get results, as do some of the other approaches I mentioned - even diet programs like Dean Ornish's have shown value.

I did read Dr Levy's book. The 'callous' analogy sounds accurate. I read about a doctor who was examing atherosclerotic arteries and he said that you couldn't scrape the plaque off, it was as if it was part of the tissue.

Sorry I didn't get the terminology quite right, VanCanada. I did know that HDL, LDL etc are carriers/transporters.


Sun Jun 12, 2011 1:32 am
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Ascorbate Wizard
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Post Re: About lp(a)
Quote:
Owen, has the lp(a) in plaque idea been confirmed by any other studies? I know Dr Rath was part of the team in the reference, but has their finding been confirmed by others?


You are right in that this is a crucial point.

In that 1990 Biesegal paper, the last line of the abstract reads:

Quote:
The possibilities for the pathways by which Lp(a) enters the arterial wall and accumulates extracellularly are discussed on the basis of the present data and recent data published by other groups.
http://internetwks.com/pauling/refs.html#R2

So this German paper would have the references you seek. I do not know whether this work has been replicated. However, I do know that before Pauling's 1990 lecture tour, there were a handful of studies re: Lp(a) and today there are multiple thousands of papers.

LDL by itself is not "sticky" without the attachment of apo(a). If Pauling/Rath are correct, and Lp(a) does act as a surrogate for vitamin C/collagen, then people with low vitamin C and low lp(a) would probably die of an aneurism before they developed heart disease.

I agree with Levy that the common denominator is low (focal) vitamin C, and that sometimes diets can make less vitamin C more effective (e.g. the paleo (no manufactured foods) diet).

I will also revise my remark - since cholesterol does not travel freely in the blood, when one speaks of cholesterol "in the blood" they speak of lipoproteins. Separating lipo from the protein is a distinction without much meaning.

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Sun Jun 12, 2011 7:51 am
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Ascorbate Wizard
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Post Re: About lp(a)
I got a little confused reading these posts. SOOOO lets go back to basics! Here's a link that explains the composition of the ever "EVIL" but necessary Lipid.
There's links that'll take back to there home page etc. to learn more.
Remember this is biased toward the medical people Ie:Statins

http://www.heartpoint.com/cholesadvanced.html

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Sun Jun 12, 2011 9:55 am
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