Dear reader: the information in this post provides the basics of Lp(a) and the details of a patient’s journey after finding out their levels were elevated a few years ago. We have converted the comments section of this post to a forum where readers can share their Lp(a) stories. Discovering that you have high Lp(a) is scary and stressful, connecting with others who are in the same boat is helpful. Nothing contained in this post is medical advice. Lp(a) is a serious medical condition and requires the care of a physician. The Familial Hypercholesterolemia Foundation maintains a list of physicians who may be able to help you make sense of elevated Lp(a) numbers.
Discovering that you have elevated Lp(a) (pronounced “lipoprotein little a”) is upsetting.
I know because I’ve had patients in this category. In this post, they relay their story.
Lp(a) production is related to inherited LPA gene variants, some of which I carry. As a result, I’ve always seen moderately elevated Lp(a) levels when I get routine blood draws. The blog post that follows highlights some of the basics of Lp(a) research, and anticipates some of your likely questions, so you can have better conversations with your physician as you decide on a course of treatment or nutrition strategy.
First, some lipoprotein basics to set the table for the rest of the conversation.
LDL-C vs. Lp(a)
Everyone has heard of LDL-C, or “bad cholesterol.”
However, LDL-C isn’t really cholesterol at all, instead it’s the measurement of the weight of the cholesterol inside of special macro-molecules called low density lipoproteins (LDL). LDL-C reflects the mass of cholesterol molecules trafficked within all of the LDL (including Lp(a) particles) per unit of volume – reported in mg/dL in the United States an nmol/L elsewhere.
Lipoproteins, of which LDL are one sub-type, carry various types of lipids throughout the body.
And even though they play a critical role in our metabolism, LDL are not our friends when they become too numerous. The European Atherosclerosis Society recently published a consensus paper calling LDL the key driver of heart disease. 1 If you are in the low carb camp and don’t believe significantly elevated LDL metrics increases the risk for heart disease, this blog post probably isn’t for you.
As a general rule, you want lower LDL-C for optimal cardiovascular health. This is the case because heart disease is lipoprotein mediated, meaning LDL are necessary for the process of heart disease to begin and progress.
As the number of lipoproteins carrying cholesterol, fatty acids, and plant sterols increases, it becomes more and more likely that one of these lipoproteins will deliver cholesterol (or a phospholipid) beneath the cells that line the blood vessels of the artery wall, where it stays stuck in place, thus setting off the inflammatory cascade that leads to heart disease. 2 The bottom line here is that the immune system doesn’t like things getting stuck beneath the blood vessels of the artery wall, and it will do its best to remove the foreign invader. However, in an attempt to dislodge the stuck particle, the immune system slowly damages the artery wall, leading to the progression of heart disease.
Lp(a) under the microscope
As you can see from the chart below, the surface of LDL particles is enwrapped by a protein called apoprotein or apolipoprotein B or APOB (the gene is APOB) for short: labs and clinicians refer to it as apoB.
There is one apoB per LDL particle.
You can think of Lp(a) as a potentially more dangerous (atherogenic) type of apoB-containing lipoprotein or LDL particle. 3
Structurally Lp(a), is a cholesterol-rich, apoB-containing LDL to which a single molecule of apoprotein(a) is bound. 4
Lp(a) testing is rare
We have seen very public examples of how elevated Lp(a) can do damage, even early in life. Celebrity trainer Bob Harper, of Biggest Loser fame, suffered a heart attack at age 52 when he appeared to be in his prime. As it turns out, the culprit was elevated Lp(a).
Although elevated levels of Lp(a) are a direct risk factor for heart disease, most “normal” lipid panels don’t even measure for Lp(a). 5
Most lipid panels done by clinicians report lipid, not lipoprotein concentrations, and hence Lp(a) measure is not provided.
In fact, when I get Lp(a) tests done my insurance carrier often sends me a letter saying the test isn’t proven and therefore isn’t covered.
In the standard lipid panel that most of us get, Lp(a) “hides” in the LDL-C number. What I mean here is that, absent a break out for Lp(a) specifically, Lp(a) will be included in your overall LDL-C number. 6 As the latest update in my Lp(a) numbers shows on the table below, I have had blood tests where my Lp(a) has been high despite LDL-C numbers that are fairly good at just over 100 mg/DL.
What constitutes “high” Lp(a)?
According to the National Lipid Association website, Lp(a) is considered elevated at levels greater than 50 mg/DL or 125 nmol/L.
There is strong evidence to suggest that elevated plasma Lp(a) levels (greater than 50 mg/dL or 125 nmol/L) are an independent – and possibly causal – risk factor for heart disease.
How I discovered elevated Lp(a)
Lp(a) first came on my radar after doing a Boston Heart Diagnostics Cardio panel. My lipid markers were generally ok, but at 43 mg/dl on one test, and with previous results at 46 and 49 mg/dl, my Lp(a) number was labeled “borderline.”
After reviewing my charts, my doctor told me there wasn’t much I could do to lower Lp(a).
“Lp(a) is genetic, you can’t change it all that much. It’s possible Niacin could help”
That’s never fun to hear for a metric that is tied to increased risk of heart disease, but I resolved to try nonetheless.
My Lp(a) results
While lowering Lp(a) through diet is certainly difficult, over the years, I have seen my Lp(a) number fluctuate. Exactly why the numbers have changed is impossible to say, but I do believe there is a link to how much dietary cholesterol I eat.
John's Lp(a) progress
The Cleveland Clinic references a study that looked at 5,000 patients with elevated Lp(a). When the LDL in these patients was brought down (not specified whether this was LDL-C or LDL-P), the “increased risk for mortality from Lp(a) was negligible.”
These are the studies that offer good news for those of us who need to keep an eye on Lp(a). Since Lp(a) is carried on the LDL particle, it needs LDL to do damage.
The less LDL to bind to, the less Lp(a).
Does Niacin lower Lp(a)?
When I first saw a blood panel that had elevated Lp(a), my doctor began discussing Niacin as a supplement, as there is some data to suggest that Niacin can reduce Lp(a) levels, although there is no evidence that Niacin reduces primary outcome clinical events in in its three major trials in persons with elevated CV-risk, and there was no event reduction even in people who saw a drop in Lp(a) when taking Niacin.
- CDP Trial – no benefit in taking Niacin
- AIM-HIGH Trial – no benefit in taking Niacin
- HPS-THRIVE Trial – no benefit in taking Niacin
The bottom line is that we have evidence that Niacin may lower Lp(a) in some individuals, but we do not have evidence it makes a difference in reducing heart attacks and strokes, and all of these trials report serious side effects in patients using Niacin.
Additional resources and key takeaways
For me, the key takeaway here is that elevated Lp(a) is a sign that an individual must be even more vigilant about maintaining proper “cardiovascular hygiene.” Although Lp(a) may not move with ease, it’s worth the effort to determine what drives your LDL-P number and make the changes you need to to get that number in line, which usually will mean less than 1,000.