Last November I published a full lipid panel on this site as part of my Fitness Journey. Most of the post was about getting my LDL down with a GLP-1 and ezetimibe. Buried in the same panel was a number I’d hardly thought about before: Lp(a), 16 nmol/L. Low risk. I exhaled in a way I didn’t realize I was holding in, and then I kept reading.
That was the easy version of the story. About 1 in 5 adults walks out of that same test with a number that should reshape how they think about the next thirty years of their life. Most of them never get the test in the first place.
This year, the cardiology establishment finally said the quiet part out loud: every adult should have Lp(a) measured at least once, full stop. Three papers landed in May 2026 that, taken together, change the playbook. I’m going to walk through what Lp(a) is, what the new evidence says, what to do if yours is high, and which “obvious” intervention turns out not to work.
If you’re 50 and you’ve never heard of Lp(a), you are exactly the person this post is for.
What Lp(a) is, in one paragraph
Lp(a), pronounced “L-P-little-a,” is a lipoprotein particle that looks a lot like LDL with one extra protein bolted on. That extra protein is called apolipoprotein(a), and it’s what makes Lp(a) different from regular LDL in two ways that matter. First, it accelerates plaque buildup in your arteries faster than LDL alone. Second, it makes your blood more prone to forming clots. Both effects compound over decades.
The other thing to know is that your Lp(a) level is set by your genes. Diet won’t move it much. Exercise won’t move it. Statins barely budge it and sometimes nudge it up. If you have inherited high Lp(a) from a parent, you have it for life, until the new drug class arriving in the next few years gives you a tool to lower it.
This is why it has to be tested once. Just once. The number doesn’t change with the seasons or the diet du jour. You measure it, you know it, and now you know whether you’re playing the cardiovascular game with a five-pound weight strapped to your ankle.
Why now: the May 2026 evidence cluster
Three things happened in the past three weeks that, individually, are interesting and, together, are a turning point.
One. Wilkinson and Koschinsky published an editorial in the Journal of Clinical Lipidology titled, without subtlety, It’s time to test all adults for lipoprotein(a). Their argument is that the 2026 ACC/AHA Multisociety Dyslipidemia Guideline now formally joins an international consensus: every adult should be tested at least once. They cite that approximately 1 in 5 individuals have Lp(a) levels at or above the risk threshold (50 mg/dL or 125 nmol/L), and that current testing rates in the general population are “very low.” Their word, not mine.
Two. Shiraki and colleagues, in JAMA Cardiology, published a pathological analysis of Lp(a) risk variants in people who died of sudden coronary death. Their work shows that the genetic variants that produce high Lp(a) are associated with specific coronary plaque morphologies and thrombus characteristics. In plain language: Lp(a) doesn’t just travel through your arteries, it leaves a different kind of damage behind than LDL does. The plaques look different. The clots that form on top of them behave differently. This is the mechanistic case for why Lp(a) is its own beast.
Three. Balling and colleagues, in the journal Heart, published a review titled Lipid-related cardiovascular risk beyond low-density lipoprotein cholesterol. The review’s framing is that the era of focusing solely on LDL is closing. Lp(a) and remnant cholesterol particles are stepping into the picture. Lp(a) is the genetic one. Remnant cholesterol is the lifestyle one, tied to obesity, insulin resistance, and the modern diet. You need both numbers to understand your actual risk.
I’m going to come back to the third paper, because it sets up an important point about what you can and can’t control. But first, what the number actually means.
What the number means, in units you can actually use
There are two units used to report Lp(a), and they are not interchangeable. Mass-based labs report mg/dL. Particle-based labs report nmol/L. The risk threshold most often cited is 50 mg/dL or 125 nmol/L. Above that, your cardiovascular risk starts climbing meaningfully.
Above 100 mg/dL the risk roughly doubles compared to people with low Lp(a). Above 180 mg/dL, you’re looking at risk levels comparable to having had a previous heart attack, even if you haven’t. That last sentence sounds dramatic, but it’s the actual epidemiology, and it’s why this number matters so much for guys our age who feel fine and have decent LDL.
In my own panel, the number came back at 16 nmol/L, well below the 125 nmol/L threshold. Lucky genes on this one. I share that not as a reassurance and not as a flex, but because I want to be clear that the case for testing isn’t “I have a bad number and you should care.” The case for testing is that you don’t know your number until you measure it, and the math says one in five of you reading this is going to find out something useful.
The 1 in 5 number from the Wilkinson and Koschinsky editorial deserves a second look. One in five. In a room of ten guys at your kid’s soccer game, two of them have Lp(a) high enough to materially change their cardiovascular risk, and probably none of them know it.
What you can do if yours is high
Here’s where the story gets honest, because the answers right now are partial.
The first thing is that high Lp(a) is not a death sentence, it’s a forcing function. If you find out at 50 that your Lp(a) is 80 mg/dL, the rational response is not to panic. It’s to get aggressive about everything else in your cardiovascular profile that you actually can move.
That means getting your LDL meaningfully low. Not borderline. Low. The 2026 dyslipidemia guidelines push toward LDL targets of 70 mg/dL for high-risk patients and below 55 mg/dL for very high risk, and “very high risk” includes elevated Lp(a) once you stack it with other factors. Statins do the work. PCSK9 inhibitors do more work if statins aren’t enough. The newer oral PCSK9 inhibitor enlicitide is moving through trials and may simplify this further.
It means getting your ApoB measured alongside LDL. A new May 2026 paper from Johannesen and colleagues in JAMA Cardiology looked at 94,398 Danish adults followed for 13 years and confirmed that ApoB and non-HDL cholesterol each carry independent risk information. If your Lp(a) is high, you want both of these numbers low. My own ApoB sits at 68 mg/dL after the GLP-1 and ezetimibe work, which is the target range, and the path I took to get there is in the Fitness Journey 4 post if you want the unsexy details.
It means standard preventive cardiology, the unsexy version. Blood pressure controlled. Insulin sensitivity preserved. Visceral fat managed. Sleep apnea addressed if you have it. Smoking? Don’t. The Balling review makes the case that remnant cholesterol, the lifestyle-driven cousin of Lp(a), is its own ASCVD driver. The good news is that remnant cholesterol responds to the things you can actually change. If you want the full menu of what aggressive prevention looks like without paying $60,000 a year for concierge medicine, I wrote it up in the DIY Longevity Protocol post.
The aspirin question, and a debunker
Here’s the part I genuinely wasn’t sure about until this month. If you have high Lp(a), should you be on low-dose aspirin?
The intuition has always been yes. Lp(a) makes your blood more clot-prone. Aspirin reduces clotting. Therefore aspirin should help. This is the cocktail-party advice that gets passed around in TRT clinics and lipidology forums and Reddit threads.
A meta-analysis by Lopes and colleagues, published May 15 in the European Journal of Preventive Cardiology, looked at this directly. Six studies, 6,628 adults with elevated Lp(a) or high-risk LPA gene variants, no prior cardiovascular disease. The headline finding: aspirin did not produce a statistically significant reduction in major adverse cardiovascular events (HR 0.60, 95% CI 0.31 to 1.17). Bleeding was numerically higher (HR 1.24, 95% CI 0.83 to 1.87). A subgroup of carriers of one specific LPA variant (rs3798220) seemed to benefit, but that finding didn’t hold up under sensitivity analyses, and the authors flagged it as likely small-sample bias.
Their conclusion, verbatim: decisions about aspirin use should be individualized and made cautiously, recognizing that current evidence does not clearly establish a net benefit or harm.
If you’ve been popping a baby aspirin every morning because you read somewhere that it was the move for high Lp(a), this is your data point to take to your cardiologist for a real conversation. It’s not necessarily wrong. It’s just not the slam dunk we thought it was.
What’s coming: the drug pipeline
The reason the testing-everyone push is happening now and not five years ago is that the drug pipeline finally has something to offer the high-Lp(a) population. Olpasiran (Amgen) is a small interfering RNA that lowers Lp(a) by about 95%. Pelacarsen (Ionis/Novartis) is an antisense oligonucleotide aiming at similar reductions. Lepodisiran (Eli Lilly) is another siRNA in trials. The Phase 3 outcomes trials for these drugs are reading out over the next two to three years, and if they show what the Phase 2 trials suggested, the calculus for high-Lp(a) patients changes completely.
One quick disclosure note, because I think it’s worth knowing. The Wilkinson and Koschinsky editorial discloses consulting and research relationships with several of the companies developing Lp(a)-lowering drugs. That’s normal in this corner of cardiology. The people who know Lp(a) best tend to be the people industry asks to advise on Lp(a) drugs. The 1-in-5 statistic and the testing-rate gap stand on their own regardless of who wrote them up.
What to do this week
Three things, in order.
First, if you’ve never had Lp(a) measured, get it measured. One blood draw. Most major commercial labs run it. Your insurance will probably cover it now that the guidelines call for it. If your doctor balks, the script is: “The 2026 ACC/AHA dyslipidemia guidelines recommend a one-time Lp(a) measurement in all adults. I’d like to get mine done.”
Second, if it comes back above 50 mg/dL or 125 nmol/L, treat that as the moment to get serious about every other cardiovascular lever you have. ApoB. LDL. Blood pressure. Sleep. Visceral adiposity. None of these will lower your Lp(a). All of them will lower your overall cardiovascular risk, which is the thing that actually matters.
Third, don’t start aspirin on your own based on the old conventional wisdom. The May 2026 meta-analysis doesn’t support it for primary prevention in this population. Bring it up with your cardiologist as a discussion, not a foregone conclusion.
If you’re under 50 and reading this, the testing recommendation still applies. Get it done in your forties, or earlier if you have a family history of early cardiovascular disease. The number doesn’t change. Knowing it is one of the highest-leverage pieces of information about your health that costs less than a tank of gas.