What’s This Little “a” Everyone’s Talking About?

If you follow health you’ll know what I mean. If not it’s just a matter of time…

Lp(a) could be a big reason we get heart attacks

Researchers have known about lipoprotein(a) for a long time and have been studying it for years. It’s now being presented as a potential big player in heart disease because the National Heart, Blood and Lung Institute just issued a statement paper on it a few weeks ago. This paper outlined what’s been done in the field and what needs to be accomplished to find out if it indeed is a problem and what can be done about it if so. Here’s a nice synopsis on it if you want a little more detail and medical-speak. It conveys a reasonable approach with admission that there’s still a lot to figure out, as the lipoprotein(a) hypothesis still needs to be tested and verified before anything is concluded or standard of care is changed.

The media picked up on this release however and we now have a new bully on the block. The reason why it’s getting so much attention is because it’s related to cholesterol and was a factor in Bob Harper’s unexpected heart attack. It’s another Waldo. We’ve zoomed in and spotted the real thing, finally. Well, we think. For some people. Maybe.

What does lp(a) mean to everyday Joe?

Lp(a), or lipoprotein(a), is one form of LDL (low density lipoprotein), a particle that carries cholesterol and other things around the body via the blood stream.

As we’ve discussed before, the best way to think about cholesterol, LDL and now lp(a), is to relate it to Venitian Handymen. Cholesterol molecules are the handymen that are doing work around the city and LDLs and HDLs are the boats that get them there through the blood stream (rivers/canals). As a general rule, LDLs are bigger boats that carry fewer handymen (cholesterol) and all their materials/tools (fat/vitamins) and drop them off at sites to build/work/repair/help/volunteer. HDLs are smaller boats that pick up handymen after they’ve done their job and take them back to the headquarters (liver) or drop them off at an LDL to do more work. Usually the HDLs are filled with mostly cholesterol because all the materials (fat, vitamins) have been delivered or used. Their name reflects this. Since they’re boats packed tight with handymen and very little fluff they’re called high density lipoproteins. LDLs are the opposite, much more fluff to carry around and less tightly packed, hence low density lipoprotein.

This brings us to lp(a).

Lipoprotein(a) is basically a type of LDL boat that, if the current thinking holds up, delivers handymen to repair sites and to fight pathogens, particularly along the walls of the canals (blood vessels). In essence, lp(a)s are boats that specialize in bring resources to repair injured cells (think artery damage). They can get stuck in the cracks and cause problems and/or oxidize, which is very inflammatory. If you have too many repair boats crowding the canals and particularly the sites needing repair forming traffic jams (plaques and blockages), this is bad news.

This is the piece that makes many people think they’ve finally found Waldo. If lp(a) boats are specifically artery repair molecules then we can get a real idea of someone’s potential risk by measuring how much lp(a) molecules they have, particularly if we can also measure arterial inflammation.

Sounds great, right?

That means we can stop worrying about cholesterol and LDL because we don’t care about all the handymen going to the thyroid, adrenal glands, brain, skin or anywhere besides the arteries. Maybe we can stop referring to LDL and HDL as good and bad cholesterol if it’s this lp(a) that’s the problem. Now we can just worry about the pesky boats/cholesterol that are designed for repairing arteries.

Not so fast…

Lp(a) levels are highly genetic and don’t seem to reflect overall health.

There’s still a ton of unknowns about it’s function and role in heart disease. Meaning if they are indeed repair focused molecules and how much they cause plaque formation and clots.

Measurements are still not regulated/consistent and testing is not common practice. Many doctors don’t know/include this in their screening and diagnosis.

Not much in drug land can help bring them down and or manage risk. This is being attended to I can assure you, and quickly.

We don’t know if lowering lp(a) does any good, particularly since it’s largely controlled by genetics.

Most importantly: this is all still a hypothesis.

This also doesn’t explain why the arteries are damaged in the first place, as hardly any of these Waldos do, which is the most important piece of this puzzle and offers a potential resolution instead of another symptom treatment.

We also need to ask ourself if driving down lp(a) is a good idea, if they are indeed the transport molecules that focus on cell repair and pathogen fighting.

It’s yet another one of those zoomed in details that explains why thy were right about it all along. When they thought it was cholesterol and that was wrong, we shifted the blame to LDL cholesterol. When that didn’t quite pan out, now they can say it actually was LDL, just that we couldn’t tell that it wasn’t all LDL, just lp(a). See, they were still right. You can trust them. 🙂

What can you take home from the latest lp(a) news?

Lipoprotein(a) is an interesting piece to the cardiovascular disease puzzle. It does offer a potentially valuable detail to uncover some of the more specifics to the disease process. A marker of how much artery repair molecules in your blood can be nice to know, particularly if there’s inflammation and/or other information on arterial damage and plaque. However, there’s still much to unfold before we can feel confident about what do with this new marker, including if there’s even anything we can do about it.

It might end up that lp(a) does cause major problems if you have a genetic disposition for it but until we are sure about all of it, we need to practice some restraint, particularly when all the phase 2 and 3 drug trials wrap up in the next couple years and the 2020 Super Bowl is sponsored by the newest lp(a) lowering drug.

So, if you or your health provider decide it might be helpful to know your Lp(a) score, have patience and don’t judge too quickly because it’s still very much the new kid on the block and we need to see what’s up with this newcomer before we run scared or buddy up.

The NY Times has a nice review on lp(a) that goes into a little more detail as well.

Thanks for reading, have a great day!

P.S. this was very simplified. There’s so much more details and nuances to this, please do more research if you want the full story. There’s a ton you can find on Google, as well as the couple links in this article.


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