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:#166  Post by Frodo » Fri May 25, 2018 1:19 pm

I had the cardio check. Nothing has deteriorated since 2017.
After my heart attack in 2016 anterio septal akinesia has been diagnosed. Akinesia has become hypokinesia. Electro cardiogram normal. LVEF 55 %. No angina pectoris symptoms. I‘m happy.
I‘ll check the lp(a) value when I‘m back at home.

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

Post Number:#167  Post by maryclaire » Fri May 25, 2018 2:22 pm

Congrats!!! Is hypokinesia better than akinesia? I looked it up and it seems so...happy to read a good report!

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

Post Number:#168  Post by Frodo » Fri May 25, 2018 2:36 pm

Yes, akinesia is dead. Hypokinesia is better, in deed.

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

Post Number:#169  Post by Frodo » Thu Jun 14, 2018 11:04 am

Paul Taylor wrote again an article about the real cause of atherosclerosis - well known in the forum:
https://www.dr.-rath-foundation.org/201 ... out-drugs/

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

Post Number:#170  Post by Frodo » Thu Jun 14, 2018 11:07 am


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

Post Number:#171  Post by Frodo » Wed Jul 04, 2018 5:22 am

owen
I‘ve got my current blood values. Lp(a) = 162 nmol/l (ref. value <75).
It‘s been at this level for six months. I don‘t know why it isn‘t dropping any further. At the moment I take about 30 grams VC, 8 grams lysine and 1,5 grams proline (and all the other nutrients).
Fortunately the „fire“ in my thyroid gland seems to be extinguished. Blood values, in particular the antibodies are OK now.
I think, there isn‘t another „fire“ else in my body.
What‘s your advice, Owen?

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

Post Number:#172  Post by ofonorow » Thu Jul 05, 2018 6:44 am

The only thing we know from experimental science is that Lp(a) becomes elevated in the absence of sufficient vitamin C. I don't know of any experiments that show Lp(a) decreases after sufficient vitamin C is introduced. There is the early "Reversibility" experiments by Willis, starting with https://vitamincfoundation.org/pdfs/WillisAthero106.pdf that showed in guinea pigs, that CVD can be reversed by introducing vitamin C back into the guinea pig's diet. This implies a reduction in apo(a) (lp(a)). We have the New York Medical professor's experience (after adding proline) and our anecdotal evidence from this forum.

Does the Lp(a) test include the particle size? Small Lp(a) are more atherogenic (dangerous) than larger molecules. And if you Lp(a) is remaining elevated, all the more reason to keep taking the Pauling/Rath Lp(a) binding inhibitors, e.g. vit C, lysine and proline.
Owen R. Fonorow, Orthomolecular Naturopath

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

Post Number:#173  Post by Frodo » Thu Jul 05, 2018 10:35 am

Johnwen
Perhaps it‘s proline. I‘d like to know how much proline you think I should take. I had my proline value measured 6 months ago. It was 212 nmol/ml and in the middle of the reference range (97-330).
I hope you‘ll give me an answer. Thanks.

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

Post Number:#174  Post by Frodo » Wed Aug 15, 2018 2:52 am

German doctor Ulrich Strunz wrote an article „News about Lp(a)“. Unfortunately only in german. I‘ll translate it later.
He reports that the annual conference of the German Society for Cardiology has dealt with the topic lp(a).
Results: Nothing new for us here in the forum. But quite interesting.

Unfortunately the cardiologists and Strunz still don‘t understand the connections. Strunz is also mistaken with regard to the limit values for lp(a). These are still 30 mg/dl or 75 nmol/l (not 75 m g / d l).

But I think my question remains exciting: Have all people with atherosclerosis high lp(a)? Has this really never been examined? This should be easy.

If there are no such studies according to which criteria have the limit values been set?

https://www.strunz.com/de/news/neues-zu ... ein-a.html

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

Post Number:#175  Post by pamojja » Wed Aug 15, 2018 9:00 am

Frodo wrote:Have all people with atherosclerosis high lp(a)? Has this really never been examined? This should be easy.


I'm sure if you search "Lp(a)+CVD" on google-scholar you would find some.

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

Post Number:#176  Post by Frodo » Wed Aug 15, 2018 9:12 am

pamojja wrote:
Frodo wrote:Have all people with atherosclerosis high lp(a)? Has this really never been examined? This should be easy.


I'm sure if you search "Lp(a)+CVD" on google-scholar you would find some.


No, I don‘t know a study. And I didn‘t find an answer to my question. Therefore I’ve asked. The answer could be only „Yes“ or „No“. Or perhaps 50%, 60% and so on...

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

Post Number:#177  Post by pamojja » Thu Aug 16, 2018 6:12 am

Frodo wrote:
pamojja wrote:
Frodo wrote:Have all people with atherosclerosis high lp(a)? Has this really never been examined? This should be easy.


I'm sure if you search "Lp(a)+CVD" on google-scholar you would find some.


No, I don‘t know a study. And I didn‘t find an answer to my question. Therefore I’ve asked. The answer could be only „Yes“ or „No“. Or perhaps 50%, 60% and so on...


Sorry, with this disease - especially with our standard of care - it is of utmost important that one also knows how to search and evaluate a health topic with such readily available tools as google. It's a little bid like in the simile: give a hungry man a fish, and he starves the next day again. But learn him how to fish, and he comes out of his poverty.

Try this most simple google search and you'll find lots of answers:

https://www.google.com/search?q=Lp%28a% ... =firefox-b

The first link is behind a paywall. Already the second gives percentages. For example:

Serum Lp(a) levels ≥ 25 mg/dL are noted in 67% of patients with rapid progression of coronary artery disease but in only 33% of patients without progression of coronary artery disease [89].


Frodo wrote:Have all people with atherosclerosis high lp(a)? Has this really never been examined? This should be easy.


Therefore the answer would be: Not all people with high Lp(a) have arteriosclerosis. And you missed an opportunity to fish for yourself. :-(


Sorry if my response sounded a bid harsh, but it was with the best of intentions. Because it is my experience that one can't rely on internet opinion. But has to learn to evaluate not only opinions, but especially the research itself. So now I would be really proud of you, if you could point it out to me, if and for which reason that percentage wouldn't be reliable.. ;-)

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

Post Number:#178  Post by Frodo » Thu Aug 16, 2018 1:07 pm

pamojja

Don‘t worry about it. And thanks for your informations.

The problem with the studies is that they are not based on the knowledge and theory of LP and Matthias Rath.
If atheriosclerosis is indeed a repair mechanism of the body in which the lp(a)-molecule is significantly involved, then the lp(a) value should be increased for all affected persons. If the value is not increased at all, the question remains why not. Are there other biological repair factors, like cholesterol, that cause deposits instead of lp(a)? I have my doubts.
Uffe Ranskov has documented this well and extensively in his book „The Cholesterol Myths“.
My doubts are also confirmed by the well known study of the Dr. Rath Research Institute with a unique animal model (transgenic mouse that cannot produce VC and instead has lp(a).
The lack of VC in the mouse has caused lp(a) levels to rise dramatically. At the s a m e time, lp(a) has deposited in the coronary arteries.

The question remains whether there are people without lp(a). According to Matthias Rath not. And in my experience not either.

Therefore: Why does lp(a) increase for me if it remains low for other atheriosclerosis patients?
That was the background to my question.
I asked Matthias Rath about it.
Perhaps I only haven‘t understand it.

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

Post Number:#179  Post by Frodo » Thu Aug 16, 2018 1:58 pm

I forgot to say:
I‘m sorry, I don‘t eat fish. :D

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

Post Number:#180  Post by pamojja » Thu Aug 16, 2018 2:06 pm

Frodo wrote:pamojja
If atheriosclerosis is indeed a repair mechanism of the body in which the lp(a)-molecule is significantly involved, then the lp(a) value should be increased for all affected persons. If the value is not increased at all, the question remains why not. Are there other biological repair factors, like cholesterol, that cause deposits instead of lp(a)? I have my doubts.


High Lp(a) is only one of many risk-factors. Some others are c-reactive protein, homocysteine, fibriginogen, Lp-PLA2, high blood pressure, insulin resistance, hypothyroid, hormone deficiency, nutrient deficiencies (vitamin C, D, CoQ10, Mg, Omega-3..).

A risk factor is only marker for possibly higher risks. It never means everyone with a risk-marker has the disease. It just becomes much more likely.

But to your question, this one particular repair-mechanism might just be impaired in some individuals. Equally as some 50% of the population aren't able or to a less extent, to metabolize folic acid into active methylfolate. We all have different bio-chemical individuality. And in lack of one repair-mechanism, there are sure a couple of fall-back mechanisms. None seems perfect, otherwise they wouldn't fail so many times.

Frodo wrote:The question remains whether there are people without lp(a). According to Matthias Rath not. And in my experience not either.


Lp(a) is a risk-marker only at higher levels. So I don''t even understand why this question has any relevance.

Frodo wrote:Therefore: Why does lp(a) increase for me if it remains low for other atheriosclerosis patients?
That was the background to my question.
I asked Matthias Rath about it.
Perhaps I only haven‘t understand it.


This question only arises if one believes that Lp(a) is the only possible repair-mechanism, or even the only cause to calcification of arteries. There is sheer stress in magnitudes of different strengths; fungal, bacterial or viral infections again in all possible combinations and strengths, and there are a multitude of repair-mechanism all working like a orchestra. Or a cacophony due to some bio-chemical individuality. Sometime one player - like very high Lp(a) doesn't plays harmoniously out of all these different co-factors in different proportions.


By the way, my Lp(a) is after 10 years still high too. But I'm not concerned because it's only a marker of a possibility. My real verified calcification of my abdominal aorta bifurcation causing a 80% blockage and 60% walking-disability has gone in remission since.

Linus Pauling patent was titled:



So high lp(a) certainly in my case, but probably in yours too, might just have been inhibited from binding. And many other factors employed with Pauling's therapy have to done the clean-up job.
Last edited by pamojja on Thu Aug 16, 2018 2:13 pm, edited 1 time in total.


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