German trying to use PT to lower Lp(a) without success

The discussion of the Linus Pauling vitamin C/lysine invention for chronic scurvy

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Frodo
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Re: German trying to use PT to lower Lp(a) without success

Post Number:#196  Post by Frodo » Thu Oct 04, 2018 11:25 am

zarfas
I am surprised your lpa value has never been measured. My value has been measured for the first time after my first cardiac arrest in 2011. It was 79mg/dl.

Shortly before that I took part in a 100km run. Without any problems. BMI 19 and body fat 8%, still today. No smoking, no alcoholics.

My current lpa value is 157nmol/l. A little less than 2011.

I think lpa is not fundamentally bad. It is an important protective mechanism in our bodies that evolved during evolution. Well explained in the articles of Pauling and Rath „Lipoprotein(a) is a surrogate for ascorbate“ and „Solution to the puzzle of human cardiovascular disease...“.

They say: „Lpa levels among individuals vary by as much as 1000 fold.“

I am interested in how and when the values vary and when and how they change.

By the way convential medicine says that the lpa gen always skips a generation. Then you wouldn‘t be affected. But I don‘t think so.

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Re: German trying to use PT to lower Lp(a) without success

Post Number:#197  Post by Frodo » Thu Oct 04, 2018 11:36 am

Sorry there is a mistake in my post.

„Shortly a f t e r I took part in a 100km run“ (not before I took part)

is the correct translation.

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Re: German trying to use PT to lower Lp(a) without success

Post Number:#198  Post by Frodo » Fri Oct 05, 2018 11:32 am

zarfas
Linus Pauling and Matthias Rath said „We observed that Lp(a) is found primarily in the plasma of those species that are unable to synthesize ascorbate“.

Most animals can synthesize ascorbate. Therefore they don‘t need Lp(a). I think you know.

But Pauling and Rath also say „There is, however, another possibility. Other animals might be found in the future with functional genes for both apo(a) and GLO. In this case, it would be more likely that plasma ascorbate levels play a regulatory role in apo(a) synthesis“.

I think there a still a lot of questions left about lp(a).

Your question „Why different units (mg/dl and nmol/l)?
Mg/dl is very doubtful and often wrong. Owen wrote about that. The better method is nmol measurement. The ref. value is <75nmol (I have my doubts about this so called reference level).

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Re: German trying to use PT to lower Lp(a) without success

Post Number:#199  Post by pamojja » Sat Oct 13, 2018 1:15 pm

And here for any possible association between Lp(a), AA, Lysine (+21% hcl) and Proline all in grams per day:
(with the caveat that I only started to test Lp(a) after starting with Pauling's therapy)

Code: Select all

year  mg/dl  AA  Lys   Pro

2009   57    7   4     1
2010   47   18   6.3   1.8
2011   59   18   6.3   3
2012   55   25   6.4   2.9
2013   43   22   5.7   1.7
2014   47   26   4.8   1.5
2015   35   27   6     2
2016   51   22   6.5   2
2017   45   25   6.4   1.9
2018   61   28   6.2   1.7

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Re: German trying to use PT to lower Lp(a) without success

Post Number:#200  Post by Frodo » Mon Oct 15, 2018 12:56 pm

pamojja
Thank you for the information.
I‘m continuing my research to get answers to my questions. Especially the relationship of lpa to atherosclerosis. (According to my survey, only one person with atherosclerosis who doesn’t have high lpa reported it.)

But also to a new question: In hibernating animals cholesterol and fats are deposited in the arteries. Although, according to Pauling/Rath, animals don‘t synthesize lpa.

I‘m still waiting for the answer by Dr. Rath.

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Re: German trying to use PT to lower Lp(a) without success

Post Number:#201  Post by ofonorow » Thu Oct 25, 2018 3:39 pm

yet, in the AA knockout mice by Rath's group, the mice expressed Lp(a)...

I think Lp(a) is apo(a) stuck to an LDL particle, so expressing apo(a) (as in the Pauling/Rath guinea pig experiments) is considered Lp(a)..

I don't know about bears, but I doubt their arteries get occluded, is that what you are saying?
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Re: German trying to use PT to lower Lp(a) without success

Post Number:#202  Post by Frodo » Fri Oct 26, 2018 10:39 am

Owen
My question:

According to Pauling/Rath in the absence of sufficient ascorbate, the human organism uses lp(a) instead to stabilize the arterial walls. If the lack of ascorbate lasts longer, this leads to the formation of plaques in the arteries.

Afterwards lp(a) is a repair material and a surrogate for ascorbate.

My question is: Then all people with atherosclerosis should have high lp(a). But that doesn‘t seem to be the case. Why?

Can deposits in the arterial wall develop without the lp(a) binding?

For example: Animals develop cholesterol deposits during hibernation, although these animals do not have lp(a).
(The animals produce less ascorbate during hibernation and do not absorb VC from the food).

Will cholesterol accumulate in the arteries without lp(a)? Then the same should apply for cholesterol as for lp(a).
I don‘t believe that and haven‘t read it anywhere.

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Re: German trying to use PT to lower Lp(a) without success

Post Number:#203  Post by ofonorow » Mon Oct 29, 2018 7:41 am

My question is: Then all people with atherosclerosis should have high lp(a). But that doesn‘t seem to be the case. Why?


I believe it probably *IS* the case, why do you believe it isn't in humans? As a thought experiment, a person on very low vitamin C (weak arteries due to deficient collagen - aka chronic scurvy) who did not make Lp(a) would soon die of an aneurysm, or outright scurvy.

I do think we know that not everyone who has a heart attack also had high cholesterol, but the lack of cholesterol (and probably Lp(a)) would have contributed to weak arteries and thus the heart attack.

The question is: Are there people who do not supplement vitamin C, and who do not have elevated Lp(a) and who are living healthy lives free from atherosclerosis? I would bet that the only way these people could exist - if they are among the few who can apparently make their own vitamin C! (overcome the GULO defect).

From the early animal experiments with cholesterol circa 1950, we learn that very high cholesterol in the diet can lead to "fatty streaks" in the arteries, but that these "lesions" were not the same as what guinea pigs (and humans) suffer without sufficient vitamin C.
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Re: German trying to use PT to lower Lp(a) without success

Post Number:#204  Post by Frodo » Wed Nov 07, 2018 11:08 am

Owen

My laboratory in Germany has written to me:
„Whether there is a way to determine the particle size of apo-a exactly is beyond our knowledge“.

My question: Is there such a possibility?

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Re: German trying to use PT to lower Lp(a) without success

Post Number:#205  Post by ofonorow » Thu Nov 08, 2018 12:25 pm

I would think that in humans, apo(a) is always attached to some LDL, and thus you want the size of the Lp(a) particle - the combination. And the size of Lp(a) is of course measurable. Atherotech used to provide a wealth of information on Lp(a) size, and thus atherogenicity
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