February is National Heart Month, so I thought I’d write a little bit about a contributor to heart disease that isn’t often discussed but affects a surprising number of people without their knowledge.

I’m not yet 50, but after a minor event last year, I found myself at a cardiologist who suggested I get a scan to check for plaque buildup in my arteries, the coronary artery calcium (CAC) test. When the results came back showing that I had “mild” build-up of calcified plaque (but enough to put me in the 90th percentile for my age), I was stunned. Sure, my LDLs and triglycerides are generally a touch high, but I’ve been vegan for over 20 years and I run 25-30 miles a week. When people asked why I ran, I jokingly told them, “I’m running from a family history of heart disease.” I guess I wasn’t running fast enough!

My great-grandfather died of a heart attack while at work. He was 75–so not “young”–but still. Another great-grandfather died at 55 of heart-related issues. In fact, the majority of that generation died either directly or indirectly because of heart disease. One generation closer, my paternal grandfather had a major heart attack at 60 and died from a ruptured aorta at 70. My maternal grandfather had a heart attack and bypass surgery at 75. My father (who is still alive and doing well) inherited much of his family’s penchant for heart disease and, as it turns out, passed it onto me as well.

I’m certainly not alone in this, as heart disease has been the nation’s number one killer for years, after the sharp decline of deaths due to infectious diseases.1 Yet, I was still confused–how could I be dealing with this at this age when I was doing so much to keep my heart in good shape?

As I mentioned, my cholesterol was a touch high, so I went on a low dose statin and it quickly brought my numbers way down. At my three month check, my total cholesterol had dropped to what my LDL alone was previously. I was in good shape. However, I’d been reading about a purely genetic component of cholesterol that is unaffected by diet and exercise and doesn’t change throughout your life. It’s been shown as a major factor in increasing risk of heart-related events. One in five people suffer from high levels, yet it’s rarely tested, perhaps because there is no solid treatment for it yet. I asked my cardiologist whether we should test for Lipoprotein(a)2 and he looked at me a little surprised before saying, “Yes. That would be a good idea.”

SciShow recently released a short video discussing how cholesterol functions, including Lp(a), titled “There’s a Third Kind of Cholesterol (It’s Really Bad).” We’re have cholesterol/protein duos that travel through our blood, with the cholesterol helping carry the protein throughout the body. LDL (“bad” cholesterol) duos are primarily cholesterol and in excess, can stick to our arteries. HDLs (“good” cholesterol) are primarily proteins and can help clear LDLs out to the liver, where they can be properly processed. And then we come to Lp(a)–let’s call it “evil cholesterol.” Interestingly, Lp(a) carries less cholesterol than other LDLs, but is more nefarious because they are small. The video explains it this way:

… they pass into the inner lining of your blood vessels. When too much builds up, you can get some nasty blood clots. LP(a)s can pull off this unfortunate trick because they look a lot like a molecule that helps break down clots in your blood vessels, but they don’t do the whole breaking down clots thing. So, when there are lots of LP(a) around, it gets in the way of your body’s clot removal systems.

Additionally, they have an extra protein called Apolipoprotein A which stick to molecules that cause inflammation and that can result in dangerous destabilization of plaque that’s built up, loosening it and increasing the risk it will break off the artery wall and stop blood flow.

There’s still more research that needs to be done on why we even have Lp(a) if it seems to have no upside. There is some thought that it “may play a role in wound healing and tissue repair,"3 but more research needs to be done.

“Normal” Lp(a), when measured in nmol/l,4 is anything under 75. Over 75 is “high” and over 100 (or, depending on who you ask, 125) is “very high.” My score? 241. Seeing that number was like a punch to the gut, especially knowing there wasn’t much I could do to lower that number at this point.

At this point, it comes down to lowering my other risk factors as much as possible. Staying on my statin, for instance, to keep my other cholesterol numbers in check. I’m running as much as ever. I cut back significantly on saturated fat and added sugars in my diet and and have bumped up my fiber intake. And I’ve reduced stress as much as I can.5

The good news is that while there are no real treatments yet, there are several in clinical trials, a couple of them in the final phases. Results have been promising: up to 95% reduction in Lp(a) and safe in the test groups with few side effects. Some of these could be ready in the next year or two. Some are injectable every few months and least one is an oral medication. Here are a few of the promising drugs being tested now:

  • Pelacarsen - It “acts like a small strand of DNA that disrupts Apo(a)-producing mRNA in the liver. Apo(a) is an important protein inside of Lp(a); so without it, your body can’t make new Lp(a).” At 80mg, it appears to reduce Lp(a) by 67-80%. Self-injected monthly.6
  • Olpasiran - Similar to Pelacarsen, but it’s a siRNA medication injected once every three months “that links with a specific group of proteins in liver cells. Together, they work to find and break apart Apo(a)-producing mRNA. This leads to a drop in Lp(a) levels.” 75+mg have shown reduction in Lp(a) of over 95%.7
  • Muvalaplin - This is the only oral treatment in trials. It has shown 70-85% reduction in Lp(a)8 by disrupting the bonding of Apo(a) to apoB, which does not allow Lp(a) to form.9

It should be noted that it has not been proven yet that lowering Lp(a) actually lowers one’s risk of heart events, but given how Lp(a) functions, I can’t imagine that there’s not going to be some positive causation (but, of course, IANAD, etc.).

I wanted to share this info to encourage you–yes, you--to ask for an Lp(a) test the next time you get bloodwork done, even if you don’t have any symptoms of heart issues.10 Any adult can test at any time and the number will be roughly the same as it’s always been. And while you aren’t able to do anything directly about it yet, knowing that you have an added risk factor will allow you to make other lifestyle changes while you wait for the clinical trials to finish up.

For additional reading…

  1. https://ourworldindata.org/causes-of-death ↩︎

  2. The “(a)” is actually referred to as “little a,” as in “Lp little a” or “Lipoprotein little a.” ↩︎

  3. Wikipedia: Lipoprotein(a) - Function and Pathology ↩︎

  4. nmol/l is the measurement of how many particles there are. Sometimes it’s measured in mg/dL, which measures the mass and isn’t as helpful. ↩︎

  5. This is a whole story in and of itself. Maybe another time. ↩︎

  6. www.goodrx.com/condition… ↩︎

  7. ibid. ↩︎

  8. www.reuters.com/business/… ↩︎

  9. https://www.ajmc.com/view/kraken-oral-muvalaplin-safely-lowers-lp-a-in-early-stage-trial ↩︎

  10. Your insurance may or may not cover this test. ↩︎