Is it Sensible to Reduce Sodium in CVD Patients?

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

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Re: Is it Sensible to Reduce Sodium in CVD Patients?

Post Number:#16  Post by ofonorow » Wed Mar 11, 2009 6:35 pm

Well, I could not retrieve the full text of that or a similar Beisegal study, perhaps they are in German but I noticed the following paper seemed to repeat the same work and was printed in a US journal and you should be able to get it. (Note apo(a) not apo(A). LDL + apo(a) = Lp(a) so this next paper is apparently an effort to clarify their claim that mostly Lp(a) is found in atherosclerosis. The history is that Matthias Rath was a medical student on the Beisegal team which did the original work. Rath was the one who made, or became aware of the connection between Lp(a) and vitamin C. That is when Rath decided to contact Pauling and told Pauling about Lp(a), and then they became collaborators. Pauling has communicated directly with Beisegal, I have a copy of one of the letters, and a major point made by Pauling in his unified theory lecture is the Beisegal team's finding of only Lp(a) - no LDL - in the atherosclerotic plaques.)

Extraction of lipoprotein(a), apo B, and apo E from fresh human arterial wall and atherosclerotic plaques
Purchase the full-text article



References and further reading may be available for this article. To view references and further reading you must purchase this article.

Tjark Reblina, Nicolette Meyera, Christine Labeurb, Doris Henne-Brunsc and Ulrike BeisiegelCorresponding Author Contact Information, a, Corresponding Author Contact Information

a Medizinische Kernklinik und Poliklinik, Universitätskrankenhaus Eppendorf (UKE), Martinistr. 52, 20246, Hamburg 20, Germany

b Department of Clinical Chemistry, A.Z. St-Jan, Ruddershove, 8000, Brugge, Belgium

c Klinik für Allgemeine und Thoraxchirurgie, Christian Albrecht Universität, Kiel, Germany

Received 14 January 1994;
Revised 31 August 1994;
accepted 28 September 1994.
Available online 16 November 1999.

Abstract

Several studies have analysed apo(a) quantitatively in arterial wall tissue derived from post mortem samples. The purpose of this study was a qualitatative analysis of Lp(a) in fresh human arterial wall tissue. It was evaluated whether Lp(a) exists as an intact lipoprotein or whether it is degraded. Additionally it was analysed whether there are differences in the apolipoprotein composition between lesion-free and diseased human arterial wall tissue. Serum and intimal tissue samples taken from the abdominal aorta and the inferior caval vein of 18 organ donors were analysed for lipids, Lp(a), and apolipoproteins apo B and apo E. Serum and tissue parameters were correlated. In the aortic tissue, higher Lp(a) and apolipoprotein levels were observed in the diseased samples. The total amount of Lp(a) recovered during three different extraction procedures was 5 μg/g wet weight in tissue free of plaque and 11.8 μg/g wet weight in atherosclerotic tissue. The corresponding values for apo B and apo E were 4.3 and 6.1 μg/g wet weight vs. 5.0 and 9.1 μg/g wet weight. After density gradient centrifugation of the aortic tissue extracts, it was shown that the major parts of apo(a) and apo B detected in the lesion-free vessel wall were present as Lp(a)-like particles. In the diseased tissue Lp(a) was partly dissociated into LDL-like particles and free apo(a). With this study we confirm that Lp(a) accumulates in the arterial wall, preferentially in diseased tissue, and that Lp(a) particles, deposited in atherosclerotic plaques, are partly degraded to LDL-like particles and free apo(a) in atherosclerotic plaques.

Author Keywords: Lipoproteins; Lp(a); Apo B; Apo E


You are right that the patent "proves" nothing, but why would a drug company patent something they claim corrects a myopathy? The history here is that Carl Folkers was an early CoQ10 researcher working for Myerck. They were aware of the effect HMG CoA Reductase Inhibitors (statins) had lowering CoQ10 levels, and you can find general agreement about this effect, (although they don't agree that this lowering harms patients), however I did find
this:

Coenzyme Q10: an independent predictor of mortality in chronic heart failure.
http://www.ncbi.nlm.nih.gov/pubmed/1901 ... d_RVDocSum
CONCLUSIONS: Plasma CoQ(10) concentration was an independent predictor of mortality in this cohort. The CoQ(10) deficiency might be detrimental to the long-term prognosis of CHF, and there is a rationale for controlled intervention studies with CoQ(10).

There is a recent petition to the FDA by Julian Whitaker asking them to add warnings to the statin drugs about the CoQ10 depletion which lists considerable literature. There are multiple studies, which led to the warnings in the Canadian NEJM.

As far as the trans fats, here is an explanation of hydrogenation http://en.wikipedia.org/wiki/Hydrogenated and note the metal catalysts used.

Metal-free hydrogenation

For all practical purposes, hydrogenation requires a metal catalyst. Hydrogenation can however proceed from some hydrogen donors without catalysts, examples being diimide and aluminium isopropoxide. Although, some metal-free catalytic systems have been investigated in academic research. One such system for reduction of ketones consists of tert-butanol and potassium tert-butoxide and very high temperatures.[15] The reaction depicted below describes the hydrogenation of benzophenone:

The claim is that not all the catalysts are eliminated, and I am trying to verify that. It is possible that I was reading about the following "side effect" in a section about the metal catalysts, and I might be wrong about the metal causing the problem, it might be the trans-unsaturated fats that are the primary issue.
The process of hydrogenation is intended to add hydrogen atoms to cis-unsaturated fats, eliminating a double bond and making them more saturated. These saturated fats have a higher melting point, which makes them attractive for baking and extends their shelf-life. However, the process frequently has a side effect that turns some cis-isomers into trans-unsaturated fats instead of hydrogenating them completely.

The exact biochemical methods by which trans fats produce specific health problems are a topic of continuing research. The most prevalent theory is that the human lipase enzyme is specific to the cis configuration. A lipase is a water-soluble enzyme that catalyzes the hydrolysis of ester bonds in water-insoluble, lipid substrates. Lipases thus comprise a subclass of the esterases. Lipases perform essential roles in the digestion, transport and processing of dietary lipids (e.g. triglycerides, fats, oils) in most – if not all – living organisms. The human lipase enzyme is ineffective with the trans configuration, so trans fat remains in the blood stream for a much longer period of time and is more prone to arterial deposition and subsequent plaque formation. While the mechanisms through which trans fats contribute to coronary heart disease are fairly well understood, the mechanism for trans fat's effect on diabetes is still under investigation.


finally, Re:
How does low serum Vitamin C contribute to higher LDL? In any case, you're citing an in vitro study as though it definitely shows that this applies to the human body.

Definitely? Not really, but we know from extensive experimentation that vitamin C controls/regulates total choesterol to 180 mg/dl. Pauling had a theory about the uptake of bile acids, but personally, after noticing this Hargood paper, the effect on HMG CoA Reductase is a theory which has in vitro evidence. No matter the mechanism, vitamin C regulates cholesterol production in humans.
Owen R. Fonorow
HeartCURE.Info
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