Heart Cipher

Ok.  So, Lp(a) is sticky and it (or its apo(a) component) can attach to inflammatory cells through the a MAC-1 dependent interface in-vitro.  But so what.  That’s just a test tube right?

But what would it mean if actual inflamed atherosclerotic plaque was examined and inflammatory cells were found to be “colocalized” with the presence of Lp(a).  Might that not suggest that this Lp(a) “recruitment mechanism” (i.e., it’s stickiness) was a critical determinant of the increased morbidity of high Lp(a)?

The authors of this study did just that.  Here’s what they have to say about it.

Lp(a)/apo(a) promotes the transendothelial migration of monocytes in a Mac-1-dependent manner, suggesting that Lp(a) and apo(a) in the atherosclerotic vessel wall may not only mediate the attachment of leukocytes, but may alsoattract these inflammatory cells to the atherosclerotic vessel wall. 5) In atherosclerotic plaques that were positive for Lp(a) expression, Lp(a) was found in close proximity to infiltrating mononuclear cells, and a high degree of colocalization was observed between Lp(a) and Mac-1,  indicating that these interactions may occur in vivo. Thus, in addition to up-regulating endothelial adhesion molecules and thereby indirectly affecting leukocyte recruitment (47),Lp(a) may directly promote inflammatory cell recruitment to the atherosclerotic plaque through its interaction with Mac-1.

So, what’s the practical implication of this colocalization of inflammatory cells with Lp(a)/apo(a) in plaque for those with high Lp(a)?

Read the rest of this entry »

In my last post, I suggested that, for high Lp(a) sufferers, a focus solely on Lp(a) volume and Lp(a) particle number was based on a specific concept of the mechanism by which Lp(a) does harm.  That is, Lp(a) does harm to the cardiovascular system by being “sticky” and adhering ITSELF to injured artery walls.

But are there other ways that Lp(a), and perhaps even low Lp(a), does harm?   Before we think about that question, some background is in order. 

• Apo(a) and LDL attach to each other to form Lp(a).  (See the graphic in the first post of this thread.)
• Lp(a) attaches itself to artery walls

One interesting question is this…  Do these two attachments take place through the same mechanism?  I believe the answer is no but I’m not 100% certain about this.

Notice, however, that there is nothing about these two attachment types that imply anything other than that Lp(a) volume and particle number need to be measured.

But suppose there was a 3rd type of attachment related to Lp(a) that was significant.

Read the rest of this entry »

It goes without saying that it’s hard to get many health professionals to take Lp(a) seriously in any way.  And then even if our health professionals will order Lp(a) tests for us, those tests will almost always only be a measure of Lp(a) volume.

The TYP program is relatively unique in that Dr. Davis emphasizes the importance of measuring Lp(a) particle number (via a Liposcience NMR test).

This is fantastic!

It seems to me, however, that there are some additional questions we need to ask ourselves.

• What is the CONCEPT underlying the view that it is only Lp(a) volume and particle number that we need to worry about?

• Is it really true that those of us with high Lp(a) only need to worry about Lp(a) volume and particle number?

Read the rest of this entry »

I just came across a study of Track Your Plaque (TYP) program blood test results for a 3 month period for a group of, hmm, let’s see, that would be one middle aged male.

Oh, yes, yes, yes that would be me!

This was no double blind with an extra twist sort of study that you’d want to give a lot of credence. But I’m sure you can imagine that it means a whole lot to me.

I wanted to get a set of baseline numbers at my HMO at 3 months on the program. I’m also looking to raise my HDL and want to participate in the new TYP program “virtual trial” of the use of PhosphatidylCholine for raising HDL. So, I needed an HDL number before I got started with that too.

There is good news and bad news in the latest results…

Read the rest of this entry »

Just a quick note.

In working on some posts about Lipoprotein(a) [Lp(a)], I came across another terrific scientific overview article about it and thought some readers may be interested in the link.

The article is entitled Lipoprotein(a): from ancestral benefit to modern pathogen?.

The article contains an interesting discussion of several theories of the usefulness of Lp(a) during the course of human evolution.

In my posts to follow (over a period of time) about Lp(a), I’ll summarize points from this article as well as the McCormick overview article referenced in a previous post.

Lipoprotein(a), also known as Lp(a) and pronounced “L P little-a”, is a type of Low Density Lipoprotein (LDL) that can significantly increase the risk of having cardiovascular disease (CVD).

And at least as I understand it, it is among the most difficult, if not the most difficult, of the lipoprotein risk factors to address with drugs, supplements, or diet. It is a genetic abnormality that is passed on from a parent having an elevated Lp(a) level to his or her children.

Too bad for me and two of my three kids then as well as about 25% of people living in the UnitedStates. For most of the period since I first realized the severity of the CVD I had, I sub-consciously believed that my only real problem was my high Lp(a) blood test value.

Stupid me. It wasn’t my only lipoprotein problem.

(images courtesy of Sally)

Read the rest of this entry »