Tuesday, March 1, 2011 at 9:28PM
Reader Kelly asks about Lp (a) in the comments.
Dr. Harris, I'm just loving the last two posts and how you relate it to Stephan G.'s recent series.
Slightly off topic, can you (or others) elaborate on why zero Lp(a) is worse than low Lp(a)? I've seen Peter mention this too but cannot find details anywhere. (My Lp(a) was nondetectable when tested last year). Is it possible to raise or is it a gene that I carry and permanent? My doctor said I'll likely never have a heart attack because of it...
The first thing to understand is that Lp (a) is not something you can do much about, other than if its high you can reduce it a bit with increased saturated fat intake. (Yeah, I know about niacin...)
This is my cartoon version of Lp (a) and atherosclerosis/ coronary events:
Lp(a) is genetically determined in that some have the increased kringle repeats and some don't. Lp(a) seems to function as a repair molecule - including vascular repair, and may relate to infection control as well.
There are two reasons you could have high Lp (a) levels, and one that you could have zero.
1) You could have lots of vascular damage going on, and the high levels would reflect lots of repair activity being required. You are the United States, with lots of crappy asphalt highways that are falling apart, so Lp (a) is the repair crews, and seeing a lot of them reflects high levels of road repair. You have repair crews and as many of them as you can muster are out fixing things because the roads are crap.
2) You could be born with a very high level, and if there is not much vascular damage going on, the high levels just mean you have a lot of Lp(a) available. You are Germany, where the roads are well-engineered high quality concrete, and the high German taxes have funded plenty of DOT repair crews - all hanging around and waiting for something to fix, just in case.
3) You could be born with very little or undetectable Lp (a). As long as little vascular damage occurs you might not need much. As long as you have good roads and keep the overweight 18-wheelers off them, you might not need a lot of road repair crews. But having some Lp (a) or some road repair crews is going to be better than none, no matter how good condition your arteries or roads start out in.
This little cartoon and road metaphor for Lp (a) fits pretty well with what the epidemiologic data tell us and with the known genetics and putative actions of it in humans and hedgehogs. In humans, it's that j-curve again. On a population basis, the lowest mortality is in people with low but nonzero Lp (a), the highest is in those with very high levels, most of whom are doing a lot of vascular damage and repair, but not all!
If you have Lp (a) that is 0, you are in category 3. The evidence I have so far is that I am in category 2. I have Lp(a) of 85 but my calcium score at age 49 is 0, my CIMT is the same as a typical 30 year old and ancestors who don't smoke (and even some with up to 50 pack years or more) typically live to the 9th decade with no coronary events. It's worth mentioning that all my relatives eat the SAD and no one has ever been diagnosed with diabetes at any age, either.
Lp(a) is a good model for how something can be a statistical risk factor for coronary events, but be relatively meaningless when applied to single individual. Of course, in my model, it is not "causing" heart attacks or anything else.
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