- What constitutes “high” Lp(a)?
- Lp(a)’s relationship to LDL-C
- How I discovered elevated Lp(a)
- How I lowered my Lp(a)
- John's Lp(a) progress
- Reducing Lp(a) risk by attacking LDL-P – still a sound strategy in light of Fourier?
- Supplements that lower Lp(a)
- Additional resources and key takeaways
Short answer – yes, you can lower Lp(a) with diet and supplements, I did, but this under the radar lipid marker is largely driven by genes and it’s tough sledding.
Talk to your doctor before taking any new course of action, but if you’re Lp(a) is really high, you may be better off targeting other metrics in addition to Lp(a), like LDL-P, that are easier to move with dietary interventions.
If you haven’t had a blood test done to check Lp(a) levels, you can find out whether you have the LPA gene by ordering a Gene Food custom nutrition plan.
What constitutes “high” Lp(a)?
Lipoprotein(a), also called “Lp(a),” has gotten a good deal of press lately as a metric to watch if you’re concerned with heart health. Elevated Lp(a) levels have been linked with an increased risk of cardiovascular disease, with the Framingham study reporting a 2 to 3 times increased risk for heart disease when Lp(a) levels are greater than 30mg/dl, or 75 nmol/L.1
However, not all medical bodies see eye to eye on what constitutes dangerous Lp(a) levels. The European Atherosclerosis Society (EAS) lists Lp(a) numbers of >50 mg/dl as elevated and as the starting point for concern.2
The Fourier trial established that Lp(a) is a risk factor for heart disease independent of where your LDL-C sits (the old thinking had been that if you get LDL-C low enough, Lp(a) becomes a non-factor).3
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).
Bob’s doctors hadn’t tested him and so he never knew he was at increased risk for heart disease.
Even had he known, could Bob have lowered Lp(a) enough to avoid a heart attack?
The subject is a matter of some controversy. Unlike other cardio related biomarkers, Lp(a) numbers are driven by genetics and are therefore tough to move with diet and drugs.
Lp(a)’s relationship to LDL-C
Lp(a) is a type of lipoprotein, which you can think of as taxis that shuttle different types of fats around the body. Lipoproteins carry triglyceride, cholesterol and phospholipids (plant fats).
In structure, Lp(a) is a cholesterol rich LDL particle that has an extra APO(a) protein added on, hence the “little a.”4
As the image below demonstrates, the “little a” is a special APOA tail that is thought to make Lp(a) all that much more dangerous.
While it is generally agreed that high Lp(a) levels are not a good thing, the exact levels considered safe is the subject of some controversy.
Most “normal” lipid panels even measure for Lp(a).
Instead, 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.5 This is an issue because it could indicate statin therapy for those who can’t reap the benefits, as Lp(a) doesn’t respond to statin therapy.
For more, see this study from Kidney International.
Since statins have no influence on Lp(a) levels, it can be expected that the LDL cholesterol-lowering effect of statins may be diminished in patients who have a pronounced elevation of Lp(a) levels accompanied by only moderate elevations of LDL cholesterol.
When LDL numbers were adjusted for Lp(a), 25.7% of the patients in the study had LDL levels that were no longer in need of statin intervention.
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.”
The conventional wisdom is no (and based on the analysis above the goal might be LDL-P more broadly anyway). As Aaron discusses below, elevated Lp(a) is determined in large part by genetics.
This is what I was told by my doctor when a blood test showed I had Lp(a) markers that were relatively high at 49mg/dl.
“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.
As you can see from the chart below, I was able to drop my Lp(a) number down to 33mg/dl by focusing on lowering my LDL-C and LDL-P numbers.
Differences in Lp(a) reporting
Interestingly, Boston Heart Labs lists Lp(a) results on its Cardio panel in mg/dl, while the Quest Diagnostics Cardio IQ panel lists Lp(a) results in nmol/L.
I had a Boston Heart panel done, and then followed up a week later with a Cardio IQ panel from Quest. I was looking for a disparity between the mg/dl number and the nmol/L number to try to prove, or disprove, the theory that nmol/L is the most accurate way to measure for Lp(a).
Unsurprisingly, my labs came back with an Lp(a) of 43 mg/dl and 98 with a nmol/L measurement, in the borderline category on both tests.
How I lowered my Lp(a)
When I first learned that I had elevated Lp(a), I was concerned. I was especially concerned because many say there isn’t much you can do to lower Lp(a).
Having said that, since I first found out about elevated Lp(a) levels, I’ve moved my number down 16 points (33%), from a high of 49 mg/dl to my new low of 33 mg/dl. Again, this is not scientific, but between blood draws, which I do every 3-4 months, I experiment with different nutritional strategies.
I am more of a lean mass hyper responder – meaning higher saturated fat diets cause my liver to make more (and clear less) cholesterol rich LDL particles. In our diet matrix, I am barely a Mediterranean, but my fat score has never been great. As a result, it’s probably not a surprise that I achieved my previous low Lp(a) number (43) after shifting to a largely plant based diet, completely getting rid of added butter (when I go out to eat all bets are off if butter is included in a dish), eating egg whites instead of the whole egg, and eating red meat very sparingly, if at all. I already eat clean, so there’s no telling whether these changes contributed to the decline of my Lp(a) number.
I achieved my 33mg/dl number after transitioning to a 85-90% plant based diet. So, essentially, I ignored most of the Bulletproof ketogenic diet themes and lowered the amount of animal protein and animal fat I was consuming. I ate Vegan a few days a week and almost always had a plant based breakfast and lunch. In short, I ate a lot less meat and a lot less saturated fat. I would still eat eggs once or twice a week, wild salmon, and some lean chicken, but I became a vegetarian for the most part.
I am not suggesting this will work for everyone, it’s just what seemed to work for me.
Notice in my data below that my best Lp(a) number (where I moved it to the green at a 72 nmol/L level) was on the same draw where I experimented with deliberately eating a junk food diet (pizza and mezcal) to see what my blood would look like. My particle count got scary high, but Lp(a) went to the lowest level ever. The 72 nmol/L is about 29 mg/dl by my estimation. The only thing I could speculate about as to why the number was so low was high doses of vitamin C I was taking at the time (1,000 mg a day), but this is obviously less than scientific.
John's Lp(a) progress
Reducing Lp(a) risk by attacking LDL-P – still a sound strategy in light of Fourier?
According to Tom Dayspring’s old work and the previous thinking was that Lp(a) wasn’t thought to be a risk factor when LDL-C was normalized.
To quote a section of Tom’s old Lp(a) paper, which actually quotes another doctor named Dr. Greg Brown:
In an analysis by Maher et al. of the Lp(a) data in the FATS trial, lowering LDL levels in those with high LDL and high Lp(a) levels dramatically reduced risk. Without treatment, these patients had a 42% risk of a major clinical event, including MI, the need for revascularization, or CV death over the 2.5 year study. When LDL levels were lowered aggressively, even though the Lp(a) levels remained high, the risk of this group was reduced to less than 10%, for a roughly 75% reduction in the risk of a major cardiovascular event. While Lp(a) (and probably risk) may be modestly lowered with niacin therapy, and with estrogens in women, aggressive lowering of LDL levels appears to be the most reliable way to treat patients at high risk due to elevated Lp(a).
This has changed in light of Fourier – meaning high Lp(a) is a risk factor for heart disease independent of LDL-C. That’s the bad news.
Important: Lp(a) increases risk pts with CHD irrespective of LDL-C. PCSK9i significantly reduced Lp(a) & pts with higher baseline Lp(a) had greater absolute reductions in Lp(a) & greater coronary benefit from PCSK9i. https://t.co/CZyCLuasLe @lipoproteinaFDN
— Thomas Dayspring (@Drlipid) December 13, 2018
BUT, the good news seems to be that the practical approach for someone with elevated Lp(a), is to aggressively target LDL-P and cholesterol rich LDL particles in particular.
So, if you’re Lp(a) is off the charts high, the consensus view seems to be that you must target the LDL-P number more aggressively.
The Maher study linked to above is from 1995. I hope to have Tom on the podcast in the next few months to get his current thinking on to what extent low LDL-C reduces the risk from elevated Lp(a).
The Cleveland Clinic references a study on this blog page, without citing or linking to it, 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).
In cases where triglycerides are high, it appears insulin resistance (and therefore triglycerides) may be the primary driver of LDL-P.
Absent insulin resistance, or perhaps in addition to issues with carbohydrate, another scenario that can rear its head is heightened cholesterol synthesis, absorption, and poor clearance. This means that some of us will make more cholesterol in response to a higher fat diet. The result is more cholesterol rich LDL-P and more risk added on top of Lp(a).
The idea here is that, in insulin resistant patients, the LDL particle is packing greater amounts of triglycerides (produced from sugar) than cholesterol. This puts the LDL-C number low, but the LDL-P, the true predictor of bad heart outcomes, high.
Taking care of the insulin resistance with metformin or dietary interventions, reduces the LDL-P count, i.e. the number of LDL-P that are moving triglycerides around. This is a perfectly logical result in those with high triglycerides (as was the case with the case study) and high LDL-P, but not as much in cases where LDL-P is elevated and triglycerides are low.
In those cases, where the LDL particles are cholesterol rich and metabolic syndrome can be effectively ruled out, we can’t rely on a “cholesterol depleted” lipoprotein theory.
In cases where the LDL-C number is high, and triglycerides are low, the method of attack is more likely to be a diet that is very low in fat and cholesterol. For more on lowering LDL-C, check out this post: Why is my LDL-C high and what can I do to lower it?
Supplements that lower Lp(a)
Lysine and vitamin C
Also known as the Linus Pauling Lp(a) protocol, this regimen calls for 3g of Vitamin C and 3g of Lysine a day.
There is some chatter indicating that Lysine and vitamin C supplementation can reduce Lp(a) numbers because lysine binds to Lp(a) particles. The lysine doses recommended sound very high to me, and I would imagine they would come with side effects for many people.
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 effectively reduce Lp(a) levels, although this study suggests that Niacin’s effectiveness may vary based on Apo(a) phenotype and it is my understanding that Niacin has generally fallen out of favor with most top lipidologists.
Consider this quote from lipid expert Tom Dayspring, M.D. from his paper titled Lp(a):
The drugs that inhibit hepatic apo (a) synthesis (niacin, fenofibrate, estrogen, raloxifene) will cause less apoprotein (a) to be attached to LDL particles. These drugs reduce Lp(a) levels but none as monotherapy are particularly efficacious as statins in reducing LDL-P or LDL-C. There are no outcome studies relating clinical event reduction to what a drug does to Lp(a) levels. There are all sorts of studies showing lowering LDL-C or LDL-P saves lives and that is why those surrogates are what NCEP strongly suggests clinician’s direct therapy at. Some advocate the use niacin to lower apo (a) levels, yet there is no clinical trial evidence whatsoever that clinical events would be affected. Many people have extremely high Lp(a) levels. Niacin can only lower it 25-30% which would never get the Lp(a) concentration close to a normal level.
What I hear Tom saying is that trials aimed at lowering Lp(a) are almost by definition performed in people with very elevated Lp(a). None of the trials in these people can normalize Lp(a) using niacin, and as a result, cardiovascular risk remains high.
It remains high UNLESS you lower LDL-P and LDL-C. Remember that the APO(a) tail has to bind to an LDL particle to be dangerous. The fewer LDL particles, the fewer opportunities for APO(a) to do damage.
So, as a practical matter, just bringing down Lp(a) is not the right call unless you are getting really serious about LDL-P.
If the Lp(a) number is only borderline high, perhaps there is a benefit in lowering Lp(a), especially if you can get levels to a normal range. Against this backdrop, it may not matter if you lower Lp(a) unless you are also lowering the overall particle count.
The bottom line here is twofold:
- Niacin supplementation has been shown to lower Lp(a) levels significantly.7
- Niacin has side effects such as flushing and insomnia.8
Omega 3 fish oil and Lp(a)
This one surprised me. As you can see from the table above, there are a series of studies that show omega 3 fish oil, sometimes alone and sometimes combined with other supplements and diet changes, lowers Lp(a).
If you’re in the market for fish oil products, check out our guide to Omega 3 fish oil, which I only half jokingly titled “Most Fish Oil is Garbage. Here’s What to do About it.”
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.
For an epic explanation of how our body’s use cholesterol, and which metrics actually matter for heart disease, I highly recommend Dr. Peter Attia’s lengthy, but excellent, series: the Straight Dope on Cholesterol.
Aaron also put together a valuable summation of the interplay between cholesterol, heart health, and genetics on this Gene Food blog, which is worth a read.
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