Can apo(B) be separated from ordinary LDL?

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

Moderator: ofonorow

ofonorow
Ascorbate Wizard
Ascorbate Wizard
Posts: 15822
Joined: Tue Nov 22, 2005 3:16 pm
Location: Lisle, IL
Contact:

Can apo(B) be separated from ordinary LDL?

Post Number:#1  Post by ofonorow » Sat Nov 03, 2018 6:47 am

Dear Vit C foundation-
The following statement on Owen Fonorow’s 2004 essay is not true. I found the study. It says nothing of the sort:

"Then, Beisiegel et. al. in Germany examined plaques post mortem and found only Lp(a), not ordinary LDL cholesterol.”

THIS is what it says: "It is concluded that both low-density lipoprotein and lipoprotein(a) have an important role in the pathogenesis of atherosclerosis.”

Here’s the link to the paper
https://link.springer.com/article/10.1007%2FBF02190527

So what’s up? Please advise.
Best,
Bob


I will stand corrected, if necessary. I used a statement made by Dr. Matthias Rath in a lecture he gave when he said that "no ordinary ldl" was found in the lesions... He was on the team. And that these results gave him the idea that apo(a) was a surrogate for vitamin C, and he left to join the Linus Pauling institute.

Here is the results from the paper you sent


The deposition pattern of both antigens in the normal intima is summarized schematically in Fig. 1 AG. In non-lesional areas there was either no staining at all (Fig. 2), or fine spot-like or a fine striped staining. Both patterns were found in the near luminal part and the near media part (Fig. 3) or were distributed over the whole area of the intima. In no case was a marked aggregation of staining observed in non-lesional areas. In contrast, in fibrous plaques and complicated lesions dense bundle-like staining pattern was seen, for both antigens. Predominant localization of both antigens within fibrous caps was seen this either reached to the luminal border of the intima (Fig. 1; CL and FP type A) or covered the necrotic core of a complicated lesion or was found at the edges of necrotic cores (Fig. 5). The distribution patterns of apo(a) and apoB in lesional areas are summarized in Fig. 1 H-L. At the cellular level


earlier

In previous morphological studies apoB has been detected in the arterial wall by means of immunohistochemistry (Hoff et al. 1977, 1978; Hoff and Bond 1983; Yomantas et al. 1984; Yamauchi and Hoff 1984; Carter et al. 1987). From these investigations it has been deduced that either LDL and/or very low-density lipoprotein (VLDL) are present. Only one study (Walton et al. 1974) has described apo(a) in the arterial wall. Interestingly, in that report it was concluded that Lp(a) does not participate in atherogenesis.


So the question is, what constitutes "ordinary LDL"? And, since Lp(a) is attached to ordinary LDL - how would you have one without the other? This was a landmark study that found Lp(a) in the plaques. Again, I went by Rath's comments on an audio tape, which I will look for and extract. Historically, at this point in research, as mentioned, only one study had looked for Lp(a)/ apo(a) and that one study had concluded it was not responsible for the atherosclerotic lesions.

It is possible that I misunderstood Dr. Rath, although "no ordinary ldl in the plaques/lesions" was his main point, as he may have meant that apo(a) was ONLY found in the lesions, as this paper suggests.
Owen R. Fonorow
HeartCURE.Info
American Scientist's Invention Could Prevent 350,000 Heart Bypass Operations a year

Johnwen
Ascorbate Wizard
Ascorbate Wizard
Posts: 2152
Joined: Sun Sep 20, 2009 5:27 pm
Contact:

Re: Can apo(B) be separated from ordinary LDL?

Post Number:#2  Post by Johnwen » Sat Nov 03, 2018 10:57 am

The LDL this person is talking about is the kind that would be found in circulation. When formed in a lesion it is oxidized and changes it’s characteristic form.

Example of this action

Surprisingly, native LDL is not taken up by macrophages in vitro but has to be modified to promote foam cell formation. Oxidative modification converts LDL into atherogenic particles that initiate inflammatory responses. Uptake and accumulation of oxidatively modified LDL (oxLDL) by macrophages initiates a wide range of bioactivities that may drive development of atherosclerotic lesions.


Here’s a link that gives the easiest to understand explanation of this process but has a $$Pharma$$ twist to it, but avoids the fact statins do nothing to control LP(a) which is the first responder to a problem!

https://www.ncbi.nlm.nih.gov/books/NBK343489/

I could post a few hundred more on the this subject but most give only a questionable sequence of the process and blame the reaction rather then the original initiating event that started the problem to begin with!
To steal ideas from one person is plagiarism. To steal from many is
research!


Return to “Heart Disease: Linus Pauling's Vitamin C/Lysine Therapy”

Who is online

Users browsing this forum: No registered users and 56 guests

cron