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Dealing with Lipoprotein(a): tests, supplements, strategy

Article at a Glance
  • Lipoprotein(a), also called Lp(a), is a lipoprotein subclass that has been linked to increased risk of heart disease when elevated.
  • Although elevated Lp(a) numbers are thought to be tied to genetics and tough to lower as a result, dietary changes and supplements like Niacin, fish oil, and L-carnitine can work for some people.

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. (R)

I was surprised to see the findings of this JAMA study which equated elevated Lp(a) with a risk for heart disease similar to having total cholesterol of 240 mg/dl, even in men under 55 years of age. However, we have seen very public examples of how elevated Lp(a) can do damage early in life. Celebrity trainer Bob Harper, of Biggest Loser fame, suffered a heart attack at age 52 when he appeared to be in the prime of his life. 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 reputed to be tough to move with diet and drugs.

Is it possible to lower Lp(a) with diet?

At least 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 I outline later in this post, my first course of action was to have a retest as I believed at the time that mg/dl wasn’t an accurate way to measure Lp(a). I have since learned that I was wrong. Many health commentators on the podcast circuit will tell you that a weight based measurement like mg/dl can register a high Lp(a) number based on large fluffy particles, which “tip the scales” and which aren’t particularly atherogenic. Instead of mg/dl, they advocate for mol/L. However, both mg/dl and nmol/L are mass based measurements, and in my case, they tracked very closely (as they will for everyone else since they mutually convert). What commentators like Chris Kresser, who is one of the ones wrongly calling for nmol/L measurements, are really trying to say is that an Lp(a) particle count is preferable to either mg/dl or mol/L since these mass based measurements could come back on the high side if the particles are large and fluffy. Lp(a) particle gives you the total number of Lp(a) particles with the potential to do damage and is therefore a greater predictor of risk, although as a practical matter, lipid experts like Tom Dayspring say that the weight based Lp(a) measurements will almost always track with the particle count. As of writing this update, I have yet to have my Lp(a) particle count done.

After the unnecessary retest, my next move was to experiment with diet. 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.

John's Lp(a) progress

 LDL-PLDL-CLp(a)Total cholesterolTriglycerides
August 201611001134917494
February 2017114710743171101
November 2017931933315766

So, we begin this post with a teaser, and an optimistic one at that: it is absolutely possible to lower your Lp(a) levels with diet and lifestyle changes.

As you move through this article, I dive more into my own experiences testing my Lp(a) levels, what supplements have shown promise in reducing Lp(a), how Lp(a) is tied to LDL, and how I was ultimately successful in lowering my numbers.

Towards the end of the post Aaron weighs in on the genetics of Lp(a).

We begin with a refresher on Lipoproteins, because if you don’t understand the basics of lipoproteins, you can’t have a good understanding of Lp(a).

Lipoproteins – cholesterol taxis

For years, dietary cholesterol has been demonized as something to avoid, but the fact is, we need some cholesterol in our diet. We need cholesterol to use vitamin D, build essential hormones, and for our brains to function properly. (R) Furthermore, most of the cholesterol in the body is made by the body, it doesn’t come from food at all. (R) Having said that, people absorb different amounts of the cholesterol they eat. One place to look to see whether you are a hyper absorber of cholesterol are the ABCG8 genes. ABCG8 is responsible for pushing out cholesterol and plant sterol that makes its way past the gut wall (the lumen) back into the digestive track where it can be excreted in bile. Thing is, the amount of cholesterol and sterol people absorb varies greatly. If you’re someone who absorbs higher amounts of cholesterol, this can contribute to a spike in LDL-C, which then makes elevated Lp(a) more dangerous according to some clinicians.

But again, dietary cholesterol itself is not necessarily the enemy, it’s how that cholesterol is transported through the body by special proteins known as lipoproteins. Cholesterol is only a problem when it clogs an artery, and it is certain types lipoproteins that take these fats and deposit them at the artery wall.

See also: Should you eat eggs everyday? No, and cholesterol has nothing to do with it

Think of lipoproteins as the yellow taxis that shuttle cholesterol around the body. They literally encase fat, just as a taxi does for a human, and deliver it to different regions of the body.

Lipoproteins have an important role to play in how the body transports fat, but not all lipoproteins are created equal. Just as there are different breeds of dog, there are different types of lipoprotein.

The two big ones are LDL and HDL.

LDL vs. HDL

HDL stands for “high density lipoprotein.” HDL sends cholesterol to your liver where it is metabolized and excreted. (R) HDL is generally labeled as good since it acts to remove unnecessary cholesterol from the body. apoA molecules are the proteins associated with HDL.

By contrast, LDL, or “low density lipoproteins” when they take a “wrong turn” can cause fat build up within the walls of your arteries, and is thought to increase the risk for heart attack and stroke. (R) (R) apoB molecules are the proteins associated with LDL.

LDL-P vs. LDL-C

It is important to know the difference between LDL-C and LDL-P if you’re going to understand Lp(a).

LDL-C, long the target of statin therapy, represents the amount of cholesterol carried by LDL in your body. You can have low LDL-C, and still have a high risk of heart disease because of LDL-P, or the total number of LDL particles in your blood.

LDL doesn’t just carry cholesterol, it also carries triglycerides, another form of fat that generally rises with sugar consumption. When blood work comes back and triglycerides are high, this can mean “cholesterol depleted” LDL, which results in low LDL-C, but elevated LDL-P. In other words, the LDL particle represents the total number of taxis on the road, not just the taxis carrying cholesterol.

It is now thought that elevated LDL-C is only a predictor of heart disease when it is concordant with high LDL-P. Low LDL-C and high LDL-P is the most dangerous territory for heart disease. (R)

With that out of the way, let’s delve into Lp(a), a great topic for our blog because Lp(a) is thought to be driven largely by genetics.

Lp(a)’s relation to LDL-C

Lp(a) is a type of lipoprotein related to LDL. In structure, Lp(a) is a cholesterol rich LDL particle with an extra Apo(a) protein added on, hence the “little a.” (R)

While it is generally agreed that high Lp(a) levels are not a good thing, the exact levels considered safe, as well as how to measure for Lp(a) is a subject of some controversy.

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, at my last test, and with previous results at 46 and 49 mg/dl, my Lp(a) number was labeled borderline.

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. (R)

We will get to Niacin and it’s ability to lower Lp(a) in more detail later on.

Measuring Lp(a) – mg/dl vs. nmol/L

As I dug into the Lp(a) research, I initially believed there was a distinction between testing for Lp(a) with mg/dl vs. nmol/L. I believed that mg/dl was a weight based measurement and that nmol/L was concentration based, and that mg/dl could be thrown off by large buoyant particles, whereas nmol/L would give you a more accurate concentration based measurement.

Some commentators argue (wrongly) that mg/dl is not an accurate way of testing for Lp(a) since the large, buoyant particles can throw off the weight and it’s the small dense particles that cause heart disease. It’s true that the small dense particles are the culprits, but the issuer is not with mg/dl vs. nmol/L. In fact, nmol/L converts to mg/dl, so both are valid. As I discussed above, the Lp(a) particle count would be the ideal and most accurate way of determining risk.

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. Again, this was an unnecessary step, but 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) (again the mg/dl vs. nmol/L is not an accurate theory).

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.

The European Atherosclerosis Society (EAS) lists Lp(a) numbers of >50 mg/dl as elevated, so my numbers wouldn’t have been considered elevated by that group, however, they are considered on the high side by most experts in the field in the US. (R)

Most people aren’t tested for Lp(a)

Most “normal” lipid panels don’t include 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. (R) 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 on this theory, 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 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 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 many 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 chicken sparingly, but I became a vegetarian for the most part.

I am not suggesting this will work for everyone, it’s just what worked for me.

Lower LDL means lower Lp(a)

There are 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). (R)

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.”

Strategies for lowering LDL-P

This does not apply to everyone, I fully get that, but the best method I have found for lowering LDL-C and Lp(a) has been eating a more plant based diet. This does not mean an exclusively plant based diet, but it does mean multiple Vegan meals a week. That dietary intervention is where I saw my greatest results thus far.

If the goal for those of us with elevated Lp(a) is to lower LDL-P count, there is a fork in the road based on whether you are insulin resistant, i.e. whether you have elevated triglycerides and blood sugar numbers. If the answer is yes, it may be better to focus on a diet that is lower in high glycemic foods.

This case study by Tara L. Dall, MD, is compelling, telling the tale of an insulin resistant woman who was able to significantly lower LDL-P by using metformin.

This study found that carbohydrate restriction reduced LDL-P in overweight men.

See also: Micro-dosing berberine as an anti-cancer strategy

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, 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)

SupplementResultStudyNotes
NiacinLp(a) decreased from 43 mg/dl to 25 mg/dlNiacin treatment of the atherogenic lipid profile and Lp(a) in diabetesStudy done in diabetic patients
Niacin / fish oil23% reduction in Lp(a)The Effects of Extended Release Niacin in Combination with Omega 3 Fatty Acid Supplements in the Treatment of Elevated Lipoprotein (a)12-week study duration also included Mediterranean diet
Omega 3 fish oil14% drop in Lp(a), 16% drop in LDL-CComparison of effects of N-3 to N-6 fatty acids on serum level of lipoprotein(a) in patients with coronary artery diseaseThirty-five male hospitalized patients with coronary artery disease were treated for 4 weeks
Omega 3 fish oilLower Lp(a)Dietary fish oil lowers lipoprotein(a) in primary hypertriglyceridemiaStudy conducted in group with high triglycerides > 250 mg/dl
Omega 3 fish oilLower Lp(a)Effects of fish oil on some parameters of fibrinolysis and lipoprotein(a) in healthy subjectsStudy looked at fibrinogen levels with long-term intake of (n-3) fatty acids
Vitamin C and LysineLowered Lp(a) from 27 mg/dl to 14 mg/dlReduction of Lipoprotein(a) in Postmenopausal WomenOne person's story over 6 months, not a large-scale study
L-carnitineLower Lp(a)The effect of l-carnitine on plasma lipoprotein(a) levels in hypercholesterolemic patients with type 2 diabetes mellitus94 high-cholesterol type 2 diabetes patients

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.

Niacin and lowering Lp(a)

The bottom line here is twofold:

  1. Niacin supplementation has been shown to lower Lp(a) levels significantly (R) (R) (R) (R)
  2. Niacin has side effects such as flushing and insomnia (R)

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.”

A note on vegetable oil and Lp(a)

Let’s revisit for a second the issue of cholesterol absorption and the ABCG8 genes I touched on at the outset of the post. Perhaps the reason I had success lowering my Lp(a) by targeting LDL-C is that I am a hyper absorber of cholesterol. In some people, the cholesterol they eat gets kicked out of the lumen by the ABCG8 genes and therefore never makes its way into the blood. In my case, I have some ABCG8 SNPs as well as elevated levels of sitosterol to prove that I am absorbing more cholesterol and sterol in general. For those of you who aren’t familiar, many lipid panels measure sterol absorption as a proxy for cholesterol absorption. Since the body makes most of its own cholesterol, we can’t use cholesterol as a marker for cholesterol absorption because it’s already there, so we look at markers like sitosterol, which is a plant fat found in foods like oats, avocado, beans, and yes, in vegetable oils. My sitosterol levels have been as high as 3.9 mg/dl, which isn’t in sitosterolemia territory, but is evidence for greater absorption. It’s generally regarded as a bad thing to be absorbing plant sterols as they are only thought to be heart healthy to the extent they prevent the absorption of cholesterol and then are kicked back out of the lumen. When they get absorbed, especially in oxidized form, as they appear in vegetable oils (which are notoriously unstable fats), they can do real damage, especially for those of us with elevated Lp(a). (R)

Why?

This NEJM study blew my mind. It teaches us that oxidized phospholipids (like we find in abundance in vegetable oils and other processed plant fats) preferentially bind to Lp(a), and it’s the combination of the oxidized phospholipids married to the Lp(a) that makes them especially dangerous.

Lp(a) – it’s all in the gene?

Why are Lp(a) numbers though to be relatively static? In part because they’re linked to genetics.

If you have elevated Lp(a), you likely inherited it, which means it’s that much more difficult to transform with diet. To explain the genetic side of Lp(a), I’m bringing in Aaron to do his thing.

Passing the mic to Aaron for this section. 

Thanks John. Lp(a) production is mainly controlled by the LPA gene. The LPA gene is one of those interesting genes which contains something called a variable number tandem repeat region (VNTR), much like MAOA which I’ve talked about previously. VNTRs are regions where a simple sequence of DNA can be repeated multiple times, with the number of repeats varying between individuals.

In the case of LPA, the number of repeats can vary between 10 and 50. In those with a larger number of repeats, Lp(a) produced from LPA is many times larger. (R) Interestingly, there is a very strong negative-correlation between Lp(a) size and its concentration in the blood (R); i.e. the more repeats in your LPA gene, the larger your Lp(a) protein and the lower your Lp(a) concentration in the blood.

Or to flip it around the other way, with fewer repeats in your LPA gene you will have a smaller Lp(a) protein but a higher concentration in the blood.

The exact reason why a bigger protein leads to a reduced concentration in the blood isn’t known, but scientists have hypothesized quite simply that a larger protein takes longer to make, and so there will be less of it produced (R).

LPA and SNPs?

There are two SNPs within LPA which are associated with an increased cardiovascular risk: rs3798220 and rs10455872.

In a similar way to MAOA neither are thought to change protein activity, rather they are thought to associate with VNTR numbers. rs3798220 or A5673G describes the switch from a ‘T’ allele to the risk ‘C‘ allele in approximately 5% of the population. Those carrying the ‘C‘ allele had increased blood Lp(a) and had double the cardiovascular risk.

Similarly, rs10455872 or T3947+467C, which describes the switch from an ‘A’ allele to a risk ‘G‘ allele was also associated with increased blood Lp(a) and an increased cardiovascular risk, although to a lesser extent than rs3798220 A5673G.

I hope that helps with your understanding of the genetics of Lp(a), as always happy to discuss any queries in the comments.

Conclusion

In conclusion, just as with nutrigenomics, where we cannot hyper focus on one SNP, there must be nuance as we examine our Lp(a) numbers as well. We know that Lp(a) is driven by genetics, but Lp(a) must bind with an LDL particle in order to do harm. For this reason, those facing elevated Lp(a) are well served in understanding what drives LDL, especially LDL-P.

In cases where triglycerides are high, it appears insulin sensitivity may be the primary driver of LDL-P. Absent insulin sensitivity, you have to really put your detective hat on to hack your own system and figure out how best to keep your LDL-P at a level where Lp(a) damage is mitigated.

Additional resources

For a different perspective on LDL, see LDL is Your Friend, by Dr. David Perlmutter (he’s referring to LDL-C).

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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53 Comments

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  1. Nate says:

    Thanks for the great info. My Lp(a) came back very high (123 mg/dl) while the rest of my lipid numbers (LDL-C, HDL, apo-B, etc) are either low or well within normal range. I am in my mid-30s and am currently in the process of seeing if I can guage if the Lp(a) number has affected my cardiac risk in any significant way. I have a cardiac CT with calcium score scheduled in the next few months and I am trying to see if diet and supplements have any effect on my Lp(a). I find it interesting that lowering saturated fat had the effect of lowering your Lp(a) considering there are multiple studies showing the opposite.

    • Nate, thanks for the comment – very interesting situation. When you say your lipids are in normal range, what were the numbers? Do you know your LDL-P?
      Wonder if it’s worth having your Lp(a) checked in nmol/L as well. As far as saturated fat, I don’t have direct causal proof that that was what lowered my Lp(a) number, and full disclosure I was still eating some coconut in smoothies, which is high in saturated fat, and some animal protein as well, but I saw Lp(a) drop as I cut out more and more animal products. When I finally started experimenting with a plant based diet, that was when I saw the dramatic drop to 33 mg/dl, which is 3 points out of the green in the Boston Heart diagnostics range. Of course, this is anecdotal, but I was shocked when my latest labs came back.

      • Nate says:

        Thanks for the response. I really appreciate it.

        My LDL-C has been around 120 over the past year, regardless of diet. My HDL-C is 40. My trigycerides went from about 75 to below 60 mg/dl when I cut down on carbs (which prior my main source of carbs were whole grains). My apo-B has been between 80-110 mg/dl and I am trying to figure out what has made it higher. I haven’t measured LDL-P directly, but I am using apo-B as a proxy.

        I did have my Lp(a) checked in nmol/L which also came out very high at 269.

        Over the past 4 months I have added in some carbs to my diet (mainly sweet potatoes), cut down on intermittent fasting, and increased my salmon intake from about 1-2 times per week to 4+ times per week, as well as added about 10-15 eggs a week to my diet. As I said I have a blood draw planned in the next week or so.

        Otherwise my diet is what most would consider a whole food diet, with a lot of veggies (10+ servings a day), chicken about 2 times per week salmon 4 times per week, and beef a few times per month. I do eat a fair amount of ghee and grass fed butter, as well as cook with avocado oil, and use a good amount of olive oil for salad dressing. You spoke of Niacin, which I have been hesitant to take unless I know the Lp(a) is indeed causing plaque or other heart health risks. I also have some Bergamot extract supplement, which I have also been hesitant to take.

        • Interesting, thanks for sharing. As I mentioned in the blog, the first change I noticed making a difference in dropping my Lp(a) levels was cutting out all butter (I had also been eating a lot of grass fed butter). Lp(a) has to respond to drops in LDL-C since it’s a combo of APOA and LDL-C. For this reason, I also eat eggs very sparingly and sometimes only the whites. I realize this is sacrilege on Keto / Bulletproof type circles, but I saw a difference. In addition, you have the whole TMAO issue with eggs that I’ve recently written about here: https://www.mygenefood.com/eat-eggs-everyday-no-cholesterol-nothing/

          Let us know how the next round of labs look, good to spread knowledge on this topic.

        • Nate says:

          I got my most recent labs back after mainly adding sweet potatoes and 10-15 eggs/week cooked in butter or ghee to an already low carb diet/whole food diet. Lp(a) increased slightly to 280 nmol/L. LDL-C increased to 137, and this is the first time I had measured LDL-P but it was higher than I would like at 1400. HDL did increase pretty substantially from 40 to 52. Triglycerides were unchanged. I have cut out the eggs and butter and plan to take your approach John for 3 months and see what the results are.

          And John maybe I missed it in the post, but what was the effect of HDL over the time period you discussed?

          • Nate,

            My HDL went to its highest its ever been at 57 mg/dl (had been 52 and 53 prior). Excited to see what happens with the plant based approach. Check back with us please.

    • Leon says:

      Hi Nate,
      I just found out that I have almost the same high LPa level as you mentioned. I was wondering what your calciumscore turned out to be and if you’re currently receiving any form of treatment.

      Thx!

  2. Jeremy Gaddy says:

    Interesting but I take issue with a few of your points, you stated that LP (a) hides in LDl-C numbers. This is not possible. They are separate particles so I’m confused. My numbers- LDL-C 112
    HDL 48
    Tryglycerides 122
    LDL-P 1250 ( optimal)
    LP (a) 365 nmol/L (super high) so I don’t see any reason for you to worry. My LP(a) level is giving me tons of anxiety. I’m 40, diet and exercise like crazy and stuck with this genetic LPa level that is very high risk. Was started on Lipitor to lower LDL c as much as possible to mitigate effects of high LP a. Will look into niacin and deal with the side effects if doctor approves. Not sure I believe the lysine and vitamin c theory. Linus Pauling is considered a whacko for this theory. Some say aspirin regimen lowers LPa. Not sure though. Hoping they are close/working on a treatment for LPa lowering.

    • Jeremy,

      Yes, when Lp(a) is not tested for it does hide out in the LDL-C number. Check out this study.

      “The usual methods to determine LDL cholesterol do not distinguish between cholesterol derived from LDL and Lp(a) and are thus the net result of cholesterol levels from both lipoproteins. High Lp(a) concentrations therefore significantly contribute to the measured or calculated LDL cholesterol levels.”

      • Jeremy says:

        Hi Andrew. I did carotid test 2 months ago and it came out fine. I’m considering cardiac CT just to gauge how bad my calcium is. Not sure a bad outcome will change any treatments though since I’m on statin already (maybe high dose) maybe adding niacin to attempt to drop LP(a) but as I said I’m planning on pushing my cardiologist to start me on it anyway. Any other ideas?

  3. Gabriella says:

    Hi John, great post. One thing I have learned about lp(a) is that people who have high levels often have a history of premature CVD in their families (men who developed it before 50 and women who developed it before 60).

    Have you looked at your family tree to see if that’s the case for you? Would also love to see another update with your numbers. My lp(a) numbers came back high — 36 mg/dL and 175 nmol/L — and I have been trying to cut back on cheese, butter and other sources of saturated fat to see how it affects my numbers. I’ve also been taking fish oil, which I’ve read can be helpful.

    Thanks.

    • Hey Gabriella, no, I don’t have any history of early CVD anywhere in my family, but interesting suggestion. 36 mg/dl isn’t an outrageously high Lp(a) number, in fact, it’s considered in the normal range by some. How did it come on your radar?

  4. John says:

    Excellent analysis and discussion on LP(a). The links throughout to other studies and articles were also very helpful. Thank you John O’Connor!

  5. amy wadsworth says:

    Hello i have ldl c of 123 hdl 93 and lpa a whopping 135 nmol/ i do 3 grams niacin daily as well as lysine, magnesium, methy b vitamins, pycogonel, lumbrokinease, vit c, zinc and NAC. i am planning to add 500 mg citrus bergamot as none of my numbers ever seem to budge..one issue my dr brought up and is insisting it could be a big part of my lpa numbers (not so much ldl) is i eat very clean )) but also consume what has always been thought of as heart healthy super dark chocolate, 85 percent pure, raw just cocoa beans and sugar in the bars…though stearic acid has been labeled as cholesterol neutral or beneficial there is science backing that steric acid but my LDL neutral but apparently has been shown to be the ONLY fat that raises LPA< other forms or sat fat have been show to raise LDL but lower lpa, where stearic acid, lower LDL and raise lpa your thoughts?

  6. Jacqueline says:

    This really has got me interested – I am 59 white female – 5’3 123 lbs, healthy and active.
    LIPOPROTEIN(a) 128 NMOL/L LDL Pattern B
    LDL Peak size 214.4 my 3 concerns
    Chol 206, HDL 109, TRI 33, LDL 88
    All my other numbers are within range – Should I be concerned and if so can I do anything?

  7. Greg says:

    I first ran across Lp(a) from Linus Pauling articles and confirmed it’s disastrous potential from a study I read that I believe was published in JAMA. In that study, I definitely recall levels being expressed in the 0-30+ ranges. I have to assume it was mg/dl, I don’t know what else it could be.
    That study of 4000 elderly white males assessed good levels as under 22, very good levels as under 11 and very bad levels as over 30.
    They participants were grouped into quintile’s The highest 20% Lp(a) group proved to have a 300% greater chance of death from all causes in the study than the lowest 20%.
    I took Lysine and Vitamin C for many years thru the 90’s in quantities for 1gm each. I had my Lp(a) checked later and it was unmeasurable. I noticed zero side effects from Lysine at all, so your comment about possible side effects is very hollow in my view and especially without you having apparently tried them.
    At age 63 after Hurricane Katrina I experienced what might be construed as chest pains and my cardiologist ordered a battery of tests including a stress test, thallium xray series and echocardiogram. he found nothing and most importantly he also found zero blockages.
    Some years later, I had my Lp(a) measured again this time by Quest and got an apparent NMol reading which at the time I did not understand except that the amounts found were infinitesimal. I had stopped taking Lysine and Vitamin C by this time.
    The article I initially read about Pauling’s experiments definitively proved Lp(a) was at the root of heart disease. In that article Pauling detailed controlled studies with guinea pigs in which he induced arterial clogging and in which he actually reversed it using Lysine and Vitamin C. Neither man nor guinea pigs produce Vitamin C internally and both suffer heart disease. Strange isn’t it? Other animals produce it internally.
    His conclusion was that an inadequate amount of Vitamin C intake for collagen production to properly repair arterial damage resulted in the body using Lp(a) to patch damage instead.
    The guy was hardly a “wacko” and put the finger on Lp(a) 25 years ago!
    The medical community spurned him because Vitamin C and Lysine were not patent-able were they?
    and there sure is a lot of money to be made treating it.

    • Donna W says:

      I have horribly high Lp(a) so I’m really worried. I guess I need to have a cardiac CT done. I had tried Vitamin C and l-carnitine for a year but it still went up. I haven’t tried niacin. I meet with the cardiologist in a few weeks, but he seemed clueless about this when I spoke with him earlier. My triglycerides and HDL are great, but LDL is too high.
      What are the side effects of Bergamot? I just don’t even know what to do at this point. I eat alot of plant foods, but have been more Paleo, so I guess I need to also cut back on meat and coconut oil (don’t have much butter already).
      Help please.

    • Deanna Gilmour says:

      Greg, can you tell me how much Vit C and Lysine you are taking? Did you start out higher and then lower the dosages as your numbers improved?
      Thanks

  8. Greg says:

    ” I do not believe that mg/dl (weight) converts to nmol/L (concentration). If I am wrong, feel free to correct me in the comments.”

    My chemist friend at NIH sent me this reply to the md/dl or nmol/L question.

    “They are both concentrations!

    mg is mass. Mole (or nmole) is used to determine relative ratios btw/ two species (stoichiometry).

    “mg” is converted to “nmole” based on the molecular weight of the species in question.

    If I have 100 mg sodium chloride, MW of NaCl is 58.5 mg/mmole, that is equal to 1.71 mmole NaCl.
    dL = .1L

    It was explained to me many decades ago why ‘dL’ is used in some applications but I forgot.

  9. Robin says:

    Hi John,

    I have a theory. First my numbers: 55 year old female 5’5″ 125lbs. Active. Walk 35-40 miles a week, Swim 1.4 miles 3 times a week and do HIIT 3 times a week. Total C 186 mg/dl, HDL 75, Trig 48, LDL C 97, Ratio chol/hdlc 2.5, non HDL cholesterol 111. LDL P number is 1127 nmol/l, LDL small is 175 nmol/ (should be less than 162 for optimal), LDL Large 7126 (should be greater than 9386 for optimal, apoA 167 mg/dl which is optimal, ApoB 75 which is optimal, and then Lp(a) 197 nmol/l. So that’s the one that sucks.

    I have been Vegan for 10 years. Eat whole foods, an occasional chip of fry but no boxed foods with tons of ingredients. Eat mostly salads, veggies and lots of organic tofu, tempeh….lots of Hemp, flax, nuts, seeds, olives….avocado oil for cooking. I found out I had high Lp(a) so I went big time low carb and dropped the fruits and quinoa, rice and potatoes. I also at 55 found out I have a little insulin resistance…which is natural as we age. My blood glucose had risen so that’s another reason I went low carb. I found a great preventive care doc and he said elevated glucose causes the inflammation that the lp(a) tries to save us from. Back in the old days, people bled to death from scurvy. Some people got lucky as time went on and developed (evolved) with lp(a) that saved them from death…by stopping the bleeding and patching the cracks in the arterial vessels. People with lp(a) lived much longer than those without it. But now, we have enough vitamin C and we should be consuming more of it! If we don’t have inflammation, lp(a) won’t be needed to put bandaids on all the cracks….doing it repeatedly builds layers of plaques which lead to all sorts of bad stuff. Does that make sense? I am taking high C, lysine, proline and few other odds and ends…in a hope to prevent any more inflammation. Maybe with no inflammation the lp(a) number just sits there and does no harm?? Kind of like the STDs that hide in the body and come out and cause issues (sores) every now and then. Also I had a Calcium score done and I got a ZERO which is fantastic (and who would have thought that?) and I did a carotid ultrasound to look for soft plaques and that report I’ll get in a couple days. Anyway, Thoughts? Thanks!!

    • Donna says:

      Robin,
      I posted in the wrong place yesterday. I was fascinated to hear you had zero in the calcium test. Can’t wait to hear about the carotid ultrasound. I have very high Lp(a) but I also have an 88 year old mom and a 93 year old dad. I would love to get them tested. I have low inflammation markers, but my LDL is too high. Need to work on that, too. What kind of Vit C and lysine do you take? I need to find a cardiologist who understands this. I would prefer not to take statins, but I am getting scared reading all about Lp(a).
      Thanks for any help.

      • Robin says:

        Wow lucky you that you have your parents still!! Must be some good genes there!! I am taking l lysine and l proline plus vitamin C (just your basic kind) and Niacin — Which has shown to lower lp(a). But again the key is inflammation. Find a preventative care doctor and get genetic testing and inflammation testing done. Make sure to do an oral glucose test. See if you have any insulin resistance…it’s a normal occurrence as we age and hormones and enzymes change. If you have early insulin resistance— you can try a low carb diet…and if that alone doesn’t lower your insulin (if it’s raised) there’s a simple medicine to help lower it.

  10. Joy says:

    I am 63 and just got tested (Acessa Labs) for Lpa and Lpb and cholesterol particle size once I learned I have the LPA gene via 23&Me genetic testing. I have had high LDL for years (genetic from my mom) but my cardiologist said no need for statins since I am vegetarian (38 yrs), walk briskly 5 hrs per week, and my heart scan shows I have zero calcium plaque. BUT, since last year my LDL has gone up from 260 to 310 (LDL 225/ HDL 57). As feared, my Lpa is quite high at 175 nmol/L and Lpb is high at 144 mg/dl. Small cholesterol particle size is normal, large is slightly low, but medium size is very high at 584 nmol/L. I saw no results on cholesterol P. I take T3 and T4 for mild hypothyroidism. Other than losing this extra 25 lbs; becoming vegan; exercising more; taking l-carnitine, vitamin C, l-lysine, niacin; and modified citrus pectin, what else should I try? I’m wondering if this is why my maternal grandfather died of a heart attack at 48. I’m feeling rather anxious since I thought I had my healthy 92 yr old father’s genes. Thank you, John and everyone who shared your stories!

  11. John says:

    What supplements are best to lower LDL-P and LP(a)? Would taking 1000 mg Niacin per day be good and does it cause liver damage and insulin resistance?

  12. Robin says:

    John,
    Great article- super helpful to me as I am 27 yo and have had a high Lpa level since I can remember! I had two questions though.
    1. Does taking ghee in coffee via bulletproof coffee formula, would that be bad for someone who has a high Lpa? I know they say ghee doesn’t elevate LDL but for someone who has high levels borderline even on medication, I don’t want to mess around but I want the benefits that bulletproof coffee has to offer!
    2. Would you want to take bergamot at the same time as that medication listed?
    -robin

    • Hi Robin,

      I can’t speak to your situation, but can say that for me, ghee and butter is a no go when I am focused on reducing Lp(a). What has worked for me is diet that is largely plant based. Based on the research that is out there, Niacin and fish oil seem like supplements worth experimenting with, but be sure to discuss with your doctor first. Good luck!

  13. Ricky says:

    I have been conducting my own self testing and you may find it interesting and counter-intuitive but please take it seriously. I had a reasonable Lp(a) in the 30’s then I went on a low carb diet and it dropped to below 10. My research indicates it is the combination of carbs and fats that lead to high Lp(a). In other words you can eat butter and meat by themselves but you can’t eat butter on a potato. I suspect french fries are as dangerous as cigarettes. Genetics, however, are probably the overwhelmingly defining factor.

    • Thanks for the comment Ricky. When I went low carb, I saw a modest reduction in Lp(a), but it wasn’t until I targeted LDL-C that I saw a meaningful reduction. What was your LDL-C and LDL-P on the different diets?

  14. Cindy says:

    I’d like to join these discussions. I’ve been working on my own N=1 for nearly 18 years now. I’ve got high Lp(a) and have worked with the Philadelphia Heart Institute (PHI) and other lipid researchers for nearly two decades. My diet has been my own modifications.

    I did my own research when the PHI recommended a different diet (AHA diet – too high in O-6 fats). My Lp(a) was 165 ng/ml at that time. I had an EBCT scan to look for calcification and the scan found nothing. I’ve had to research and figure out my own diet, but now I’m wondering, like John, if it’s time to consider a vegetarian diet. I’m happy to share my numbers, comments from my cardiologist (a research lipidemiologist from MUSC) about diet, and my own anecdotal evidence. And I’m looking for motivation to experiment once again with diet.

    For information — I achieved my best numbers against all predictions from the PHI at age 65 when my TC reached 197 and my Lp(a) reached 14 ng/ml. My diet consisted of an egg in the morning, some sauteed greens like spinach (coconut oil) mid morning, 3 – 4 ounces of salmon around noon, and a salad with olive oil by 2pm. I was using Intermittent fasting without knowing it back then. But I also was walking 7 or 8 miles 3 or 4 times a week, lots of hills (felt like HIT), and I lost a lot of weight. Carbs minimal. No grains, no processed foods, and no bad oils. I supplemented with high doses of D3 and K2.

    I don’t know where to begin. At this point, my status is that I do not have any calcification according to a recent EBCT scan (age 71), do not have any cardiac symptoms (considered asymptomatic Lp(a)), take 2G of niacin ER daily, have very good blood work all around, according to my cardiologist (excellent IR, HbA1c, LDL particle size, HDL).

    But I’m interested in experimenting with less animal saturated fats, more veggies, and some supplements. I’ve seen the research on saturated fats regarding how they lower Lp(a), but wondered whether this is animal or vegetable saturated fats. I cannot get enough Omega-3 from wild caught Pacific salmon and my cardio doc suggested supplements for this. I just started these. She herself takes those herself in the form of Carlson’s fish oil.

    So I hope this is a viable form and I can learn more. ~~ Thanks, Cindy

    • Cindy, thank you so much for the thoughtful comment, quite interesting. In particular, the research on saturated fat you mention is definitely food for thought, although if you have to sacrifice high TC for high Lp(a), maybe not worth the switch? Did you have your LDL-P measured through this process? Please keep us updated with your progress.

      John

      • Cindy says:

        Thanks for the reply, John. I did have the LDL-P measured and my numbers are really low risk, according to my cardiologist – in the lowest category. She is really surprised by the low LDL-P and even IR. As it turns out, when I drop my Lp(a), my TC also drops as do both LDL and Trigs. My highest TC occurred when I was vegetarian, but I think that is because I relied on grains (and some bread) and beans for the main portions of the meal. Since then, I sprout my beans before cooking and avoid breads and grains.

        I’m really curious as to whether you’ve had good luck with lowering Lp(a) by eating whole grains. This is still a gray area for me. Also, do you think the saturated fats from a food like avocado works to keep the Lp(a) down? Currently, I try to balance out any saturated fats I eat each day, try to keep quantities down, including nuts.

        But I think there are other factors to the elevated Lp(a). I cut calories and dropped about 15 lb, as well as lowered the HbA1c from 5.7 to 4.9. I walked 35-40 miles per week on hills. I believe that my pretty much avoiding mammal saturated fat except for salmon and halibut from Alaska (3-4 oz 4 or 5 times a week) and the daily egg may have had something to do with these better numbers. And I started taking the Niacin and D3 with K2 (10,000 IU of D3). I don’t think this is a monolithic process.

        The doctor at PHI also thought that my inclusion of red wine 4 or 5 times a week contributed to the lower Lp(a). I know drinking alcohol is controversial over all, but I suspect that a strong exercise program and healthy weight might keep the alcohol from doing a lot of damage. So much about genetics here, I guess.

        Now I’m trying to figure out the next stages with Lp(a). If I do not take my 2G of Niacin ER daily, my TC will begin to creep up as will the LDL and Lp(a). But I’ve never had a reading as high since the original reading of 165 ng/ml. Since age 65 when I did that turnaround, my highest Lp(a) reading has been about 20.

        Are you exploring any dietary changes?

        Thanks, Cindy

  15. Ann says:

    Thanks for this article and comments!
    Yes, LP(a) can be reduced with Linus Pauling protocol!
    My total cholesterol has been consistently high 294, with HDL of 103, LDL 178, triglycerides 64. I eat low carb and exercise. After reading Dr Linus Pauling’s research, I had my LP(a) tested and it was 55 nmol/l which is below the 75 nmol/l limit-but I wanted to see if I could lower it. My Dr kept insisting that my high total cholesterol was genetic and must be reduced with statins. I agreed with the genetics, not the statin therapy. I started on the Pauling protocol, 2000 mg Vit C, 1000 mg L-Lysine, 1000 mg proline 3 times per day…no side effects. After 4 months my LP(a) test is now 38 nmol/l! I intend to test to ascertain if this regimen has impacted my cholesterol scores in the near future.

  16. Stacy says:

    What about using Lipase enzymes? Couldn’t that be effective in breaking it down? I just had my genetic testing done and out of the 27 snps I am +/+ for 24 of them. Big wake up to the LPL. Overwhelmed in how to approach this, but you have given a start and things to look into. Thank you!

  17. Cathy says:

    Like you, John, I got dramatic 33% lower results when I changed to vegan. My Lp(a) dropped from 90 to 68 to 59 over 11 months, as measured by the Boston Heart Test. … For 20 years, doctors denied that my chest pains indicated a heart problem because I was so fit & all tests were good. Finally one ordered the Calcium CT scan: a whopping 327: CVD. (Personally I attribute it to the tablespoon of saturated coconut oil I’d added to my oatmeal for 2 years at the recommendation of ill-informed friends.) Good, knowledgable doctors, including cardiologists, are v. hard to find.
    I did Dr. Dean Ornish’s 9-week “Reversing Heart Disease” program, which is covered by Medicare & many insurance companies (because it works). It takes some discipline. No meat, fish or dairy (I do non- fat cottage cheese & yogurt, tho, to stay above 90 lbs.! .. Weight melts away.) Also limited to a max. of only 10 grams of fat/oil/day. A smart cardiologist put me on time-released Niacin (no side effects).
    On the basis of my own research, largely from Life Extension, I also take lysine-proline, algae-based Omega-3 + DHA, Alcar & Turmeric. (Will bring back the Vit. C I’d been taking now after reading your posts here.) A nurse told me she’d seen positive results reversing plaque with 360 mg. of Vitamin K2-7per day. Supposedly takes almost a year before you want to re-test your
    Cal CT score.

  18. Jayne says:

    Hi, Thanks for all the info. I had my LP(a) tested for the first time and it’s a terrifying 215. My CRP score is 10.3 as well. I work out (strenuously!) take fish oil, and eat mostly low carb with good fats. My Good cholesterol has always been a bit high throwing off the total cholesterol but recently my LDL got up to 147 and triglycerides are 85. I’m trying to determine what diet to follow as I’ve gotten conflicting advice. I’ve just added sublingual B12 and niacin. Do you have any suggestions for supplements,diet, and even pharmaceuticals? at this point I’m pretty nervous. Thanks!

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