Diet and Lp(a)

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

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Frodo
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Diet and Lp(a)

Post Number:#1  Post by Frodo » Sun Jan 27, 2019 6:30 am

Owen

Someone has asked me in a german forum:

„If VC deficiency, damage to blood vessels and high lp(a) are related, then why do my husband and daughter have high lp(a) and I do not? Especially since our diet is the same.“

Owen, can you help me with an answer?

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Re: Diet and Lp(a)

Post Number:#2  Post by ofonorow » Sun Jan 27, 2019 9:17 am

Great point, and illustrates the fact, not only of biochemical individuality (we are all different in so many ways) but that the problem of Lp(a) is mostly genetic, evolutionary new development, meaning there is a great difference among us, and Lp(a) is not responsive or based on diet.

This is from one of the Pauling/Rath US patents (# 5,278,189)


Essentially all human blood contains lipoprotein(a); however, there can a thousand-fold range in its plasma concentration between individuals. High levels of Lp(a) are associated with a high incidence of cardiovascular disease. Armstrong, V. W., et al. (1986) Atherosclerosis 62: 249-257; Dahlen, G., et al. (1986) Circulation 74: 758-765; Miles, L. A., et al. (1989) Nature 339: 301-302; Zenker, G., et al. (1986). Stroke 17: 942-945 (The term occlusive cardiovascular disease will be used hereafter as including all pathological states leading to a narrowing and/or occlusion of blood vessels throughout the body, but particularly atherosclerosis, thrombosis and other related pathological states, especially as occurs in the arteries of the heart muscle and the brain.)


Prevention and treatment of occlusive cardiovascular disease with ascorbate and substances that inhibit the binding of lipoprotein (A)
http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&p=1&u=%2Fnetahtml%2FPTO%2Fsearch-bool.html&r=1&f=G&l=50&co1=AND&d=PTXT&s1=5278189.PN.&OS=PN/5278189&RS=PN/5278189

Now, the Pauling/Rath guinea pig experiments illustrated that Lp(a) (really apo(a)) rises in these vitamin C deficient animals after being deprived of their ordinary dietary vitamin C - leading to atherosclerosis, based on the sticky Lp(a). The latest Rath-team work with GULO-knockout mice (mice that cannot make their own vitamin C) illustrates the same thing. Lp(a) adapts the body for low vitamin C by increasing and thus strengthening otherwise weak arteries.
Owen R. Fonorow, Orthopath® (Orthomolecular Naturopath)
® is a trademark of the Institute for Orthomolecular Studies

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Re: Diet and Lp(a)

Post Number:#3  Post by Johnwen » Mon Jan 28, 2019 12:54 pm

What Owen said here is accurate but also another component of the Pauling protocol which is lysine is also a very important part when it comes to LP(a).
LP(a) is a scavenger which is in constant search for dead tissue within the circulatory system when it comes upon an area that has dead tissue it rapidly attaches to it. If the tissue etc. is not attached it takes and attaches to it and transports it back to the liver for removal. If the tissue is attached it locks on to it and recruits other fats in circulation to either feed the surrounding tissue and heal it or to cover it up so it won’t allow the dead tissue into circulation.
Sometimes the covering becomes excess and builds to a blockage.
Lysine in the circulatory system looks like dead tissue and LP(a) readily attaches to it. Then both are processed out! This in turn slows the covering process so the V-C and other components can nourish and heal the damaged area. The liver keeps a army of LP(a) in circulation and this balance is maintained so if some are removed more are produced to keep the balance so it it’s important to keep a steady state of lysine to counter act the high balance and regulate what is in play!
The only thing right now that has been shown to lower this production is Niacin. Since the drug co.s aren’t making $$ from it there are some that are working on drugs to do the same thing.
Since the drug co.s aren’t able to profit from it right now, it is a ignored fact and medical people aren’t educated on the pitfalls and actions of this component. Now you take a look at Statins an that’s BIG$$ for the Pharma people so they push it out and the problem still remains. Reading the latest theory’s on how the clogging of arteries works is like reading, “The green men from mars invading your blood!”

So in this situation taking PT is a daily must! Adding Niacin to their supplements can only help in the long run! Finding the causative factor that is influencing these high levels can and is a elusive factor especially with the way today’s medical people are taught! One factor I can think of right now is a question. That being does this person get cold sores??
To steal ideas from one person is plagiarism. To steal from many is
research!

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Re: Diet and Lp(a)

Post Number:#4  Post by Frodo » Tue Jan 29, 2019 4:10 am

Thanks, Owen and Johnwen!

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Re: Diet and Lp(a)

Post Number:#5  Post by Frodo » Mon Feb 11, 2019 11:45 am

The answer from the Rath-Team - abridged and translated:

„The human body is very complex. There is always an interplay of numerous factors to consider. For this reason, nutrition should not be considered as the sole factor influencing lp(a)-concentration.
Some factors influencing lp(a)-concentration:
- The constitution of the entire body Are there any illnesses? Some illnesses can increase lp(a), others can decrease. Especially the gastrointestinal tract is crucial. How much VC does arrive in the cell at all?
- The genetic make-up (Inheritance of higher or low values)
- The intake of drugs. For example certain antibiotics.
- The lifestyle. Especially smoking and stress.

You see how many factors are influencing. Even if you and your family eat the same, your body can react completely differently.“


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