102.  That’s my number.

Yup- that’s my total cholesterol levels.  Not just HDL (high density lipoprotein cholesterol, or “H”ealthy), but also LDL (low density lipoprotein cholesterol, or “L”ousy).  But, as I’ve often said, these are surrogate measurements.  Because we hadn’t identified the proper substance that indicates our chances for heart disease or cardiac complications.

Research demonstrates that HDL has heart protective effects; that’s really why it’s called “good” or “healthy” cholesterol.    HDL binds toxic compounds in the blood, helping excess cholesterol get excreted from the body.  (Interestingly, these effects don’t seem to be true for those folks undergoing dialysis- either peritoneal or hemo-dialysis).

It’s those facts that led me to search out other theories.  That’s how I found the work of Dr. Robert Krauss, now at UCSF, who devoted his research to plasma lipoprotein research and cardiac disease,

Dr. Krauss identified that there were four different type of bad cholesterol.  Using ion mobility analysis, he found that the smaller, denser versions of LDL correlate more closely with heart disease than the total LDL levels.  This was especially true for those subjects who have low levels of HDL (good) cholesterol.

This finding explained why those folks who take drugs to lower their cholesterol (and actually manifested lower cholesterol levels) still manifested cardiac complications.  And why those who don’t take drugs (and their total LDL levels are horrendous) still die of heart disease.

That was a decade ago.

Now, we know a little more.  Lipoprotein (a) [Lp(a)] a form of LDL, is probably the exact culprit we’ve been seeking.  Produced by the liver, it contains another sliver of protein [apoliprotein(a)], that makes it pretty sticky.

Oh, and not surprisingly, given what I’ve already told you here, at least 80% of the Lp(a) levels in our body are strictly a genetic issue.  Yup- it’s already present in our bodies when we are tykes of 2- not waiting until we are older, when we start worrying about heart disease.  By the time we are five- we have pretty stable levels of Lp(a) that maintain themselves over the courses of our lives.

So, what is it about Lp(a) that creates the problem?   It either causes or augments the formation of plaque, those deposits on the inner layers of our blood vessels,  which diminishes blood flow.  It’s that stickiness factor that helps plaques form and stick to the walls of the vessels.

Those of us who manifest elevated Lp(a) levels actually have a much higher risk for heart attacks (by 50%) and 2X the risk of suffering a stroke.

OK, you say.   How can we target drugs to reduce the levels of Lp(a)?  I say drugs, because we’ve already found that exercise, diet, BMI (body mass index) doesn’t correlate with Lp(a) levels.  So, it would seem that we need something to eliminate this from our bodies.

Well…

We also don’t have data demonstrating that lowering Lp(a) levels cuts the risk of cardiac disease.

But, if you live in Europe or Canada, testing for Lp(a) levels (at least once) is the norm.  Not so in the States.  (Whether that’s because we have no treatment to sell folks if they find they have higher Lp(a) levels or because we can’t provide that we can lower the Lp(a) levels and reduce our cardiac risks is up for debate.)

So, while this goes on, we keep taking those statins.