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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, 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 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 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.

John O'Connor

John O'Connor is the founder of Gene Food. He is passionate about nutrition, genetics, and wellness and uses this blog to publish self experiments as well as some of the research that the Gene Food team does internally to highlight stories of bio-individuality.

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71 Comments

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  1. Heidi Thompson says:

    I see a clinical lipidologist at UCSF in 2 weeks. Curious what can be some to help my numbers. 45 years old. 5’4” 130#
    TC 302
    HDL 60 😇
    Trg 134
    LDL 213
    LP(a) 287 nmol/L
    Statins and I have never been friends.

  2. Stella says:

    I’m an active 55 year old female. 5’6 120 pounds. My father died of heart attack/stroke at 45. I have these results.
    HDL 95
    Triglyceride 67
    LDL 99
    LPA 129.
    Due to family history I am quite freaked out by the LPA, Doctor had wanted to put me on a statin but I’m afraid of side effects and now it seems a statin does not even work for the LPA? I’m confused and freaked out. Please advise.

  3. Eric says:

    Just received my lp(a) labs today after seeing my LDL-C incrementally go up over the past few years from 100 to 127 (although two weeks after the initial tests, now 120??). Anyway, the following are my latest numbers and general info:

    38 yo male; 160 lb, 5’7″, non-smoker, decent diet at the moment could be better but not horrid; exercise moderately (cardio machines, tennis, hike with dogs etc.). Overall fairly healthy

    lp(a): 402 nmol/l
    LDL-P: 1414 nmol/l
    LDL-C: 120 mg/dl
    HDL-C: 43 mg/dl
    HDL-P: 25.1 umol/l
    TG: 115 mg/dl – up from 100 2 weeks ago
    TC: 186 mg/dl – down from 195 2 weeks ago

    From talking briefly to my primary physician who prescribed a low dose of statins (haven’t taken any yet), and reading on the internet, it is apparent that my lp(a) numbers are insanely high, the LDL-C and LDL-P are in the borderline higher range and the HDL values could be a bit higher. As far as I am aware there isn’t any family history of heart issues other than my great grandfather had a heart attack, but he smoked like a chimney. My dad is taking prazastatin sodium, but his numbers are good for the most part; unsure of his lp(a), however.

    It seems that is is worth making significant modifications to my diet and see what that does. Do you guys have any other thoughts, recommendations? Is being on a statin regimen worthwhile? I am planning on seeing a cardiologist in the near future to get more input. . This is a little overwhelming at the moment.Thanks for any insight.

  4. ben says:

    My doctor says I’m an enigma..

    The ratios all look very good
    TC/HDL = 3.3 (300/90)
    TG/HDL = 0.67 (60/90)
    ApoB/ApoA1 = 0.62 (123/197)

    But there’s heart disease history in the family.. so he wants to use a statin (Atorvastatin) to see if he can lower the Lp(a) of 88 nmol/L and TC of 300.

    Any thoughts if I should first check to see the % blockage using the Coronary Calcium Score and/or a carotid ultrasound?

  5. Don N. says:

    John excellent article,
    I was diagnosed with extensive blockages on all 3 arteries and ended up having stents – June 2018.. My Lipid panel always had been within range(upper level). I’m in good physical condition, regularly exercise and age 47. Since the stents I’ve been put on a high dose of statins. Last December I was checked for LPa and found to have very high level at 175 nmol/L. I have been on a strict vegan diet since August/2018. I did my blood work a week ago and found to have LPa at 767mg/L ( 191 nmol/L). Rest of my lipid panel is ultra low: Cholesterol 1.4 mmol/l; LDL 0.5mmol/l; HDL 0.71mmol/l; non HDL 0.7mmol/l; Risk Ratio 1.99; Triglycerides 0.45 mmol/l; Just like you mentioned I was very optimistic of being a vegan but now at a loss with these results. Very much appreciate any thoughts.

    • Hey Don, a couple thoughts. First, usual caveat, I am not a doctor, goal here is to spread info that will help aid communication with health care providers. However, there is a study out of SD finding that Lp(a) increases with oxidized phosholipid (oxPL) intake, and from what I gathered, it seemed to say that oxPL were a factor in serum Lp(a) levels. I quote a NEJM study above showing that Lp(a) binds preferentially to oxPL. So…if you are absorbing sterol at an accelerated rate, perhaps that increased absorption is driving the high Lp(a) levels? What are your sitosterol levels? The plant based heart guys (Esselstyn for example) are not just Vegan guys, they are very anti sterol as well, but that never gets reported. They don’t want nuts, seeds, oils, avocados because presumably their patients are all hyper absorbers and when those sterols oxidize, they get bad outcomes. In that regard, you can look at sterol plus HbA1c to see if there is glycation / oxidation stemming from a glycemic response.

      However, having said all that – many clinicians believe low LDL-C takes all the teeth out of the Lp(a) problem, so you might be on the right track regardless. I would try having the sterol discussion with your doc and seeing what he / she says.

      John

      • Don N. says:

        Thanks John. I strictly follow Esselstyn diet, so technically I shouldn’t have high levels of Steriols. My HbA1c is 5.7%. My GP is not aware of checking steroils in blood work so will have to wait until I see my cardiologist in 2 months. I have not been taking any fish oil as Esselstyn diet don’t recommend any of that. I’m in doubt whether I should take any. Also another interesting point – I’ve been referred by a Cardiologist from South Asia stating that a herbal supplement consisting of 3 plant ingredients(named Thripala consisting of “Aralu, Bulu and Nelli”) known to reduce LPa in South Asians. I’ve been taking it for the last 2 months but there is no visible change in LPa. Wish I could get to the bottom of this.
        Thanks again!

  6. Lin says:

    Thanks to all,
    More information than I have been able to find anywhere else on LP(a) issues. I am a 61 year old very healthy woman. After reading Peter Attia’s articles and podcasts, I decided to test my LPa (against my primary care physician’s judgement). I was shocked to see an LPa level of 255nmol/l ! Yikes!!!!!! My Triglycerdies have always been low 42, HDL 73, calculated LDL 91. My glucose is low IGF1 low and have never had any health issues. I exercise a few hours a day and eat healthy. Haven’t tried any special diets for any extended period. I’m having a Coronary Calcium Test Thurs.

    I have read in some studies that even if your LPa is high, as long as your Trigycerides are low, it shouldn’t be a coronary risk but none of us want to take that gamble. Like the rest of you I am scrambling to try and figure out something I can do to avoid a cardiac event.

    I will keep reading here and really appreciate all the information. Thx!

  7. Joy Segars says:

    Do check your liver enzymes when taking daily niacin. Once daily Rugby brand extended release 500mg/day niacin lowered my high Lp(a) by about 15%, so my doc said to take it twice a day. I decided to check my liver enzymes because I’d read that niacin can negatively affect them. My liver enzyme markers for inflammation were high enough that my doc said to go back to niacin once per day. In the meantime, 500mg of citrus bergamot (Jarrow) daily lowered my high LDL by 50 points, so I recently started taking it twice daily. Has anyone tried that? Next I’m adding in berberine for further cholesterol control. Has anyone had good results from that? Thanks John and everyone!

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