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LIPOPROTEIN(a):
THE UGLY CHOLESTEROL
Lipoprotein(a), abbreviated as Lp(a), is
composed of one molecule of LDL, the bad cholesterol, chemically bound to a
carrier protein called apolipoprotein(a). Lp(a)
is an adhesive particle, and in health serves to repair and restore the
structural integrity of a damaged blood vessel wall -a
sort of biological super glue. It’s
apolipoprotein(a) component promotes blood clotting and inhibits your body’s
blood clot dissolving system. This
is Mother Nature’s mechanism to prevent excessive blood loss from a damaged
vessel. Lp(a) also promotes vessel
wall cellular growth and proliferation, and its LDL cholesterol is incorporated
into the regenerating cells. Essentially,
Lipoprotein(a) is a repair molecule, an “artery patch”.
Vitamin C can also serve to maintain or restore
the wall strength of our blood vessels, rendering Lp(a) unnecessary,
A dog the size of an average man will convert dietary sugar (glucose)
into 20,000 mgs. of Vitamin C each day. We
will see that this is nature’s preferred approach.
Man, the great apes, guinea pigs, and hedgehogs lost the ability to make
Vitamin C from sugar, and rely on Lp(a) instead to keep their arteries intact.
Man and these other species do develop coronary artery disease.
All other animals make Vitamin C; Lp(a) is not found in their blood, and these
animals never develop coronary disease. These
Vitamin C producers do not obstruct their blood vessels with
cholesterol and blood clots!
During the Ice Age, agriculture ground to a halt and
natural fruits and vegetables were in short supply.
Animals that could manufacture their own Vitamin C could handle this, but
mankind began to die off from blood loss anemia.
Without Vitamin C, we developed chronic scurvy; blood leaked out from our
damaged arteries and we had no way to repair our vessels or to stop the
bleeding. Evolution than provided
mankind with a solution. A genetic
mutation of plasminogen, the circulating protein that promotes blood clot
dissolution, created apolipoprotein(a), a plasminogen look alike that does just
the opposite, promoting blood clot formation and antagonizing plasminogen
mediated clot dissolving. Apo(a)
plugged the hole in the dike. Combined
with LDL to form Lp(a), it restored the strength of our vessels.
Individuals who couldn’t make Lp(a) died; those who could make Lp(a)
survived the Ice Age and passed on their
Lp(a) producing genes to their descendants.
This is why some Lp(a) is present in all of us.
Lp(a) obviously saved mankind from extinction during the Ice Age, but
what is this cholesterol/clot producing patch system doing to us now?
2.
The role of Lp(a) in vascular disease.
After the Ice Age, dietary Vitamin C became
plentiful again, our vessels were strong, and Lp(a) vascular “repair” was
not needed. Our Vitamin C intake was at “animal” levels and mankind did not
experience coronary disease. With
the advent of modern day food processing, we are again becoming Vitamin C
deficient, and in our current “diet induced Ice Age”, we are again calling
upon Lp(a) to patch up and repair our arteries, and today we call that patching
system ATHEROSCLEROSIS.
Lp(a) levels are under hereditary control; if your level is high, that
is because your ancestors needed more to get them through the Ice Age.
The higher your level, the greater is your risk.
Lp(a) binds to lysine and proline within the wall of a damaged or
weakened artery, depositing its LDL and promoting the deposition of circulating,
oxidized LDL into the artery’s
wall, narrowing the artery. Lp(a)
promotes the formation of blood clots on top of the cholesterol plaque, abruptly
narrowing the artery further, bringing on or worsening your symptoms. If the
clot is large enough, it will occlude the artery, producing a heart attack.
We now know that most heart attacks are due to a large blood clot
developing in vessels with moderate narrowings (therefore you are still at risk
with a 50% narrowing).
Lp(a) levels typically range from 1 to 100; the highest level so far in
our practice has been 200. Mg. for
mg, Lp(a) has 10 times the plaque producing potential of LDL.
The average American value is 14: 13 in healthy individuals and 19 in
coronary patients. Lp(a) selectively
accumulates in your arteries; a level above 30 doubles your risk, and if your
LDL is also elevated, your risk rises by a factor of 5.
Lp(a) also concentrates in the walls of your bypass grafts; 90% of
individuals whose bypass grafts clog up have Lp(a) levels above 31.
Balloon angioplasty (PTCA) is basically a
controlled trauma to the vascular wall, and Lp(a), always a “repair”
molecule, will concentrate at the site of balloon dilation, promoting clot
formation and cholesterol deposition. You
certainly won’t be surprised to learn that Lp(a) has been implicated as a
cause of restenosis, renarrowing of the blood vessel following angioplasty. In
one study, the Lp(a) level averaged 7 in patients who did not renarrow, and 19
in those who did. Those patients
with a level above 40 were 11 times more likely to restenose than those with
levels below 4. Those with levels
above 19 were 6 times as likely to renarrow.
3.
What can I do to lower my Lp(a) related coronary risk?
Plenty:
A. Have
your Lp(a) level measured (along with your other risk factors).
B.
If
your level is elevated, work with your doctor to lower it with Niacin
C. The
Lp(a) that cannot be lowered can be neutralized by supplemental Lysine and Proline.
By occupying the binding sites on the circulating
Lp(a) particle, Lysine and Proline prevent
Lp(a) from attaching to Lysine and Proline within the
vascular wall, and if the Lp(a) cannot attach, it cannot promote
cholesterol deposition and blood clotting within the coronary artery.
In optimal doses, Lysine and Proline may be able to insinuate themselves
between bound Lp(a) and the vascular wall, freeing up
Lp(a) and
pulling it out of the vascular wall. The now freed-up
Lp(a) will take
cholesterol out with it, lessening the degree of
vessel narrowing.
D. To
learn more, please attend our next “The
Ugly Cholesterol - Lipoprotein (a) and Vitamin C” talk. Eradicating Heart Disease and Why Animals
Don’t Get Heart Attacks, by Mathias
The Vitamin C and Pycnogenol pages also provide information related to Lipoprotein(a) James C. Roberts MD FACC