Question on PT theory

[farside]

The PT theory (as I understand it):

1. The inside of the artery wall gets damaged (various causes).
2. Lysine binding sites in the damaged arterial wall get exposed.
3. If not enough Vitamin C around, the body uses LPa to seal the arterial wall cracks. This works because LPa has a lysine binding site.

So once the LPa has attached to all the exposed lysine binding sites in the arterial wall, no more lysine is exposed, so the LPa should not be attracted anymore to the damage site. But evidence is that the thin film of LPa keeps building up. Why?
If LPa was attacted to LPa, large clusters of LPa would form in the blood and would fall out of the blood as a precipitate. I believe that doesn't happen.

So why does the damage site keep on getting larger?

Also, if enough Vitamin C was available to the body, how would it go about properly repairing the arterial wall (i.e. not use LPa for the repair)?

Thanks!

[johnjackson]

Yes!!
Lpa should be attracted to other Lpa, before the Lpa is attached to the membrane!
and then get solid and come out of the blood, or form a clot?

so when Lpa is attached to a LBS on the artery wal, why does more Lp(a) attach to it?

maybe there is some conformational change to the lp(a), once it binds to the wall. that allows other Lp(a) to bind to it and the binding sites that attaches to the wall?

I'm interested

[farside]

maybe there is some conformational change to the lp(a), once it binds to the wall. that allows other Lp(a) to bind to it and the binding sites that attaches to the wall?

I suspect not - if that were the case, then lysine in the blood that binds to circulating lp(a) would make the lysine+lp(a) combination sticky and it would grow and precipitate out.

Just in case anyone misreads my intentions here, I am not trying to falsify or denounce PT, just trying to dig deeper into what is really going on. I am relying on PT to save my life!

Also the other question I raised : "if enough Vitamin C was available to the body, how would it go about properly repairing the arterial wall?". I guess this is what happens with big cats, but what exactly does happen?

I have other questions too:
a) How does lysine in the blood unstick lp(a) that is already bonded to the damaged site?

b) Once all the lp(a) has been unpicked from the damaged site, are we not back to where we started, an exposed damaged arterial wall lining (i.e. we have unpicked the scab, so will it start bleeding? ) I suspect this is where Vitamin C comes in, but I haven't seen a full explanation.

[johnjackson]

I know enough to know that it isnt vit C that does anything, except to make collagen.(in the case of repair to not need lp(a))
so your big question,

"if enough Vitamin C was available to the body, how would it go about properly repairing the arterial wall?".

vitamin c is the limiting recant to make collagen

like "limeys" on long boat rides, it wasnt the vit C from limes that prevent scruvy, it was the vit C to make collagen that did it.

[farside]

Yes, Vitamin C + Lysine makes collagen. Somehow the body does this when sufficient VC etc are available. So that leaves the queries:

1. Why does lp(a) keep building up after the exposed lysine receptors in the damaged arterial wall have been filled?
2. How does lysine in the blood unstick lp(a) that is already bonded to the damaged site?

[Lone Dog]

I always thought the Mike Ciell write-up of the PT was a good one. I haven't read it for a while though, so I don't know if it answers the questions. Maybe no-one knows, and medical science doesn't concern itself with the PT. Here it is if you haven't seen it...

http://www.ourhealthcoop.com/pdf/MikeCi ... theory.pdf

These days I'm finding the PT a bit simplistic, and thinking one has to start considering atherosclerosis in more detail, regarding inflammatory processes, macrophages gorging on cholesterol, calcification etc. Maybe PT works fine in the early days of the plaque, if it is comprised largely of lp(a). If your problem is ldl-laden plaque, perhaps it won't. Just a few thoughts.

[johnjackson]

Lone Dog:
good point and why K2 is much needed
The following article is how we know of vitamin K's role in regulating arterial calcium:

Vitamin K protects the heart
http://www.lef.org/Magazine/2000/2/report/Page-01

Vitamin K regulates calcium

Imagine a vitamin that could keep calcium in bones and out of arteries. In so doing, that vitamin could stop heart attack and osteoporosis at the same time. Sound incredible? Maybe, but research shows that vitamin K does exactly that. It works by regulating calcium. Bones need it, arteries can't stand it. Vitamin K accommodates both.

viewtopic.php?f=11&t=11891

[farside]

[Lone Dog]

Imagine a vitamin that could keep calcium in bones and out of arteries. In so doing, that vitamin could stop heart attack and osteoporosis at the same time. Sound incredible? Maybe, but research shows that vitamin K does exactly that. It works by regulating calcium. Bones need it, arteries can't stand it. Vitamin K accommodates both.

I recall an old post from Johnwen, regarding how vitamin K does the job, but to speed it up you need vitamin D3, which promotes the removal of calcium from soft tissues. Then vitamin K deposits that calcium into bone. I think these are a good addition to the PT.

[Lone Dog]

https://www.nmcd-journal.com/article/S0939-4753(11)00227-4/pdf

Figure 2: Areas with diffuse intimal thickening contain high quantities of proteoglycans that capture lipoproteins. The retained lipoproteins trigger an inflammatory response, which in turn further increases the lipoprotein retention by the release of bridging molecules and the stimulation of proteoglycan production. Consequently, lipoprotein retention is part of a vicious circle that ultimately leads to a maladapted inflammation and atherosclerosis.

This takes us into a further level of discussion. What if those proteoglycans didn't capture lipoproteins, but blocked their retention, maybe even repelled them?

I have Dr Levy's book STOP AMERICA'S #1 KILLER, which includes a section on Chondroitin Sulfate (CS). Basically, it says that sulfur/sulfate repels lipIds. If the proteoglycans are connected to highly sulfated chains of CS (rather than forms which didn't have much sulfate, and which might attract lipids), the connective tissues, and ground substance of the arteries are able to resist, or repel lipids. This is a simple explanation, but you get the gist of it.

Here's an article about CS...

https://www.drugs.com/npp/chondroitin.html

If you search the forum, you will find some threads about CS. A couple of links worth checking out are as follows. The 1st shows a report from a doctor about the reversal of atherosclerosis in the eyes of patients taking CS. The 2nd shows how CS does the same in an animal study. The latter is quite complex in places, but worth persevering with. I also enjoy the photo showing the clean-looking arteries!

Another good addition to the PT.

https://drrichardstalksback.wordpress.c ... n-sulfate/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6238215/

[farside]

Amazing info on CS, Lone Dog.
Definitely add this to the arsenal!

Two questions:
- Can you take CS and also do PT at the same time?
- What form of CS is best : bovine, marine or avian ?

[DiverDown2]

Tower Laboratories "Asccorsine-9" includes Chondroitin sulfate in their formula.
So yes you can take CS with PT at the same time. Which should be a great addition.

[Lone Dog]

Two questions:
- Can you take CS and also do PT at the same time?
- What form of CS is best : bovine, marine or avian ?

I don't see why you couldn't take them at the same time. You'd think the effect of one would support the effect of the other, and maybe even speed up that effect. Dr Levy says Vitamin C may improve the quality, sulfur-wise, of the CS in the arteries. I've seen some studies here and there which even say VC increases the body's own production of CS.

Dr Levy refers to Chondroitin Sulfate-A (CSA), and Chondroitin Sulfate-C (CSC). He says either one is of benefit. The latter appears to have a higher sulfate content, generally. If you look at the work of Dr Morrison, he used CSA. I believe CSA can be had via bovine sources. As for CSC, I can't find any corroboration, but I think this comes from marine sources.

[ofonorow]

Revisiting the original post.

The PT theory (as I understand it):

1. The inside of the artery wall gets damaged (various causes).
2. Lysine [and proline] binding sites in the damaged arterial wall get exposed.
3. If not enough Vitamin C around, the body uses LPa to seal the arterial wall cracks. This works because LPa has a lysine binding site.[and proline binding site - University of Chicago)]

So once the LPa has attached to all the exposed lysine binding sites in the arterial wall, no more lysine is exposed, so the LPa should not be attracted anymore to the damage site. But evidence is that the thin film of LPa keeps building up. Why?
If LPa was attacted to LPa, large clusters of LPa would form in the blood and would fall out of the blood as a precipitate. I believe that doesn't happen.

So why does the damage site keep on getting larger?

I think we do know by now that large clusters of Lp(a) do not form, however the first Pauling/Rath patent informs us that the size and mass of Lp(a) varies in different individuals by 1000 fold.

First, taking "sufficient" vitamin C, lysine (and proline) plaques do not expand, and we have evidence that the arteries become "clean." https://pdfs.semanticscholar.org/8f16/2551a4087f384f901f48ba50ef2dd94b93a8.pdf

For example, the Pauling/Rath have another patent for cleaning organs of atherosclerosis prior to transplant. The organs are dipped pre transplant in a vitamin C and (lysine) solution. The plaques literally melt off the organs.

So your question is why does the film keep building, under ordinary (low vitamin C) circumstances. At least part of the reason must be the lack of vitamin C, lysine and proline leading to more instability in the artery. As other posters have mentioned, Dr. Levy in STOP AMERICA'S #1 KILLER explains the process of forming atherosclerosis in detail without relying on Lp(a) as the primary sticky culprit.

Also, if enough Vitamin C was available to the body, how would it go about properly repairing the arterial wall (i.e. not use LPa for the repair)?

Thanks!

The answer is found among all the animals that do not make their own vitamin C - and generally do not suffer the same type of heart disease (if any) that we humans do. The arteries with sufficient collagen stay strong, stable, do not crack.