Lipoprotein(a)
Makes the News
Is the
mainstream finally catching up with Linus Pauling/Matthias Rath?
Copyright © 2000
Owen R. Fonorow
On
September 4, 2000 the news briefly appeared that should have sent shock waves
through the entire medical-pharmaceutical industry. Researchers at Oxford University were about to publish their
paper in the American Heart Association journal CIRCULATION with their findings that
people with high levels of lipoprotein(a) are 70% more likely to have a heart
attack than those with lower concentrations.
In 1990, Linus Pauling and Matthias Rath singled out lipoprotein(a)
(small “a”, Lp(a) for short) as the dangerous variant of LDL (“bad”)
cholesterol that causes heart attacks, strokes and plaque build-ups on the
walls of arteries.
The
AP news report “Lipoprotein Ups Heart Attack Risk” by Troy Goodman Associated Press writer, while exciting to this author personally, did contain inaccuracies or misleading statements. Whether or not these distortions were
intentional, what follows is an attempt to set the record straight. For example, there are now more than 1200 published scientific papers on what
the news report called an “obscure” cholesterol particle. The news report implied that in the previous
decade, researchers had not been able to link high Lp(a) to an increased risk of heart attack in the
general population. The news report
claimed that the reason doctors don’t normally screen for Lp(a) is because no
standardized screening exists. The AP
report repeated the often made claim that Lp(a) is not alterable with drugs or
changes in diet. Finally, the AP reported
that Lp(a)’s exact role in the blood is unknown. At least one statement made in the report is true. There are no known prescription drugs that
can lower Lp(a) levels.
Lp(a)
is an ordinary LDL cholesterol particle with a sticky apoprotein particle
called apo(a) attached to its surface. Medicine has known, at least since 1985,
that Lp(a) forms atherosclerotic plaques, not ordinary LDL. The Brown-Goldstein Nobel Prize in Medicine
of that year first brought the so-called cholesterol Binding Sites to the
attention of medical researchers.
Researchers figured out that Lp(a) binds to lysine strands that become
exposed after the wall of the artery suffers a sore or lesion. Yet for reasons unknown most people, many
doctors and the mass media never picked up on this important work and the
variant cholesterol Lp(a) has been lumped together with ordinary LDL.
Linus
Pauling became interested in Lp(a) after research in Germany confirmed that
plaque deposits on human aortas was entirely Lp(a) and not ordinary
LDL.[1,2] A member of this German
research team, Matthias Rath, came to the United States to join Linus Pauling
after he realized that Lp(a) based plaques were an evolutionary counter-measure
for the chronic low levels of vitamin C in human beings. In other words, Lp(a) operates in the blood
as a surrogate for vitamin C [3].
An
important finding that impressed both Pauling and Rath is that the “sticky”
Lp(a) particles have only been found in the few animals that do not make their
own vitamin C, including humans. Most beings make vitamin C in their livers or
kidneys in very large "mega" amounts by current medical standards;
they do not have Lp(a) in their blood, and rarely do they suffer cardiovascular
disease (CVD). Humans are almost unique among life on Earth in that they must
get vitamin C entirely from the diet.
|
Group |
Endogenous Vitamin C |
Lp(a) in the Blood |
CVD |
|
Humans |
No |
Yes |
Yes |
|
High-order Primates |
No |
Yes |
Yes |
|
Guinea Pigs |
No |
Yes |
Yes |
|
Other 99.9+% of Species |
Yes |
No |
No |
Pauling
and Rath were also impressed by the observations of Canadian doctor C. G.
Willis in the 1950s. Willis noticed
that plaques generally formed in locations where blood pressure is high, e.g.
in the coronary arteries near the beating heart. If cholesterol was the cause, and not the effect of heart disease
they wondered, why aren’t these plaque formations and infarctions more randomly
distributed throughout the body?
Pauling
and Rath performed experiments at the Pauling institute with one of the few
animals that does not make its own endogenous vitamin C (the guinea pig) and
proved that there is a connection between vitamin C and Lp(a) in these animals,
and probably humans as well [4]. When
vitamin C in the guinea pig’s diet is “adequate” (roughly 3-5 gm per day in
human terms) the pig does not suffer atherosclerosis. Lp(a) levels remained constant. These were controls. Pigs in the other group had their vitamin C
limited to the U. S. RDA equivalent. These pigs uniformly began to suffer
atheroslcerotic plaque build-ups.
Importantly the Lp(a) levels in this group of pigs became elevated.
The
Pauling/Rath unified theory holds that heart disease is the body’s healing
response to chronic scurvy. A much
slower form of acute scurvy that killed sailors without fruits on the high
seas. Scurvy and CVD is caused by a
lack of collagen in the body. When
vitamin C levels are adequate, collagen production is ample and arteries remain
strong and pliable and do not suffer many lesions or injury. In humans, and the few other species that do
not make endogenous vitamin C, blood vessels tend to weaken because collagen
production is limited. Lp(a) levels
rise in response to low vitamin C. The
elevated Lp(a) causes the plaques to form over the blood vessel lesions and
are, in Dr. Rath’s words, “Nature’s plaster casts.”
It
is true that Lp(a) is not generally screened for in ordinary cholesterol
testing and that special procedures are necessary to get accurate
readings. Contrary to the AP report,
there are companies that can accurately measure Lp(a) at a very reasonable
cost. One company, Atherotech of
Birminghan Alabama (www.atherotech.com), offers their VAP® test across the country, if
not world-wide. Atherotech will send their testing kits without charge. The kit
includes complete lab instructions that explain how to process the sample
before returning it to Atherotech for analysis. Atherotech not only measures Lp(a), they break it into 5
subgroups.
A
recent danger is that your Lp(a) reading may be computed (estimated) based on
other cholesterol levels, rather than measured. The FDA has approved these computations (guesses) on the grounds
that it is difficult to measure Lp(a).
The FDA has decided that because
there is “nothing” currently available (meaning a prescription drug) that is
known to alter Lp(a), there is no real need to accurately measure it. This is
nonsense. Because of these new rules,
people will see their Lp(a) numbers and not know if they are measured (real) or
computed (estimates). If you are
concerned about your heart attack risk, make sure your Lp(a) is measured and
not computed. Atherotech offers “gold
standard” Lp(a) measurements with their VAP tests.
Because
no prescription drug or low-fat diet has been shown to alter Lp(a) it is
generally held that this molecule is a genetic factor. Dr. Pauling stated that,
"if you have more than 20mg/dl of Lp(a) in your blood it begins to deposit
plaques, causing atherosclerosis." According
to Dr. Rath, studies show that special
diet does not influence Lp(a) blood levels. However, vitamin C and vitamin B3
(niacin) can lower blood levels of Lp(a).
Vitamin B3 probably acts on Lp(a) production in the liver, while vitamin
C levels, according to the Pauling/Rath theory, attack the root cause.
Furthermore,
significant documentation attests that Vitamins belong to the most powerful
agents in the fight against heart disease. This fact has been established by
studies of thousands of people over many years:
.
Here are some important results of recent clinical studies:
·
Vitamin
C cuts heart disease rate almost in half (documented in 11,000 Americans over
ten years)
·
Vitamin
E cuts heart disease rate by more than one third (documented in 36,000
Americans over six years.)
·
Beta
Carotene (provitamin A) cuts heart disease rate almost in half (documented in
36,000 Americans).
Pauling
said the following about the use of Vitamin C and lysine to counter the Lp(a)
risk:
"Knowing that lysyl residues are what causes
Lp(a) to get stuck to the wall of the
artery and form atherosclerotic plaques, any physical chemist would say at once
that the thing to do is prevent that by putting the amino acid lysine in the blood to a greater extent than it is
normally. You need lysine to be alive,
it is essential: You have to get about 1 gram a day to keep in protein balance,
but you can take lysine, pure lysine, a
perfectly non toxic substance in food , as pills, which puts extra lysine molecules in the blood. They enter into
competition with the lysyl residues on
the wall of arteries and accordingly count to prevent Lp(a) from being deposited, or even will work to
pull it loose and destroy
atherosclerotic plaques." Linus Pauling, Journal of Optimum
Nutrition, Aug 1994
The
Vitamin C Foundation has conducted a small pilot study to test individual
reports that nutritional products can markedly lower Lp(a) levels in
humans. The study seeks to verify
reports that products high in vitamin C, lysine, proline, vitamin E, vitamin A,
carnitine, etc. do have dramatic impacts on Lp(a) levels. As of this writing the average decline in
Lp(a) from eight subjects who had been given free product is 68%. In at least two cases, Lp(a) levels in the
blood initially rose about 10-20%, before they began recording significant
declines. The Foundation hopes other
researchers and laboratories will conduct more controlled clinical studies on
these effects at the high doses Linus Pauling recommended. This pilot study is
on-going and for current results, please refer to:
http://www.vitamincfoundation.org/lpastudy/vcfltr.htm
For
more information on the Pauling/Rath Unified Theory or to obtain a video tape
that Linus Pauling made on this subject in 1993, visit www.PaulingTherapy.com.
Correspondence:
Owen
R. Fonorow
Intelisoft
Multimedia, Inc.
PO
Box 3097
Lisle,
IL 60532
Fax:
1-630-416-1309
fonorow@foxvalley.net
1.
“Lipoprotein(a)
in the arterial wall.”, Beisiegel U; Rath M; Reblin T; Wolf K; Niendorf A, Eur
Heart J 1990 Aug;11 Suppl E:174-83
2.
“Morphological
detection and quantification of lipoprotein(a) deposition in atheromatous
lesions of human aorta and coronary arteries” [published erratum appears in
Virchows Arch A Pathol Anat Histopathol 1991;418(1):86], Niendorf A; Dietel M; Beisiegel U; Arps H;
Peters SWolf K; Rath M, Virchows Arch
A Pathol Anat Histopathol 1990;417(2):105-11n R.
3.
“Hypothesis:
lipoprotein(a) is a surrogate for ascorbate”,
[published erratum appears in Proc Natl Acad Sci U S A 1991 Dec
15;88(24):11588], Rath M; Pauling L,
Proc Natl Acad Sci U S A 1990 Aug;87(16):6204-7
4.
“Immunological
evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion
of the hypoascorbemic guinea pig.”, Rath M; Pauling L, Proc Natl Acad Sci U S A 1990
Dec;87(23):9388-90 Arch A Pathol Anat Histopathol 1990;417(2):105-11n R.