Lipoprotein aMeasurements of lipids levels are frequently used to assess the risk of future coronary heart disease or stroke. These two disease conditions are commonly termed cardiovascular disease (CVD).

Blood levels of total cholesterol, triglycerides and high density lipoprotein cholesterol (HDL-C) are measured when assessing a standard lipid panel. These numbers are then used to calculate low density lipoprotein cholesterol (LDL-C), which has been found to be strongly correlated with the risk of CVD.

Recently measures of lipoprotein particles involved in atherosclerosis, which is the main underlying cause of CVD, have been found to be very useful to assess risk. Examples of such measurements are LDL particle number (LDL-P), apolipoprotein B and lipoprotein(a).

Although lipoprotein(a) or Lp(a) is a strong risk factor for CVD, the lack of clinical trial data have resulted in Lp(a) being largely ignored by clinical guidelines assessing the prevention of CVD.

In 2010, the European Atherosclerosis Society (EAS) consensus panel recommended screening for elevated Lp(a), in people at moderate to high risk of cardiovascular disease. Desirable Lp(a) levels < 50 mg/dL were considered a treatment priority, after therapeutic management of LDL-C.

According to a statement from the EAS;

… the evidence clearly supports Lp(a) as a priority for reducing cardiovascular risk, beyond that associated with LDL-C. Clinicians should consider screening statin-treated patients with recurrent heart disease, in addition to those considered at moderate to high risk of heart disease. 

What Is Lp(a)?

Lipoproteins are the particles that transport cholesterol and triglycerides in the blood stream.

Lipoproteins are composed of proteins (apolipoproteins), phospholipids, triglycerides and cholesterol.

The lipoproteins vary in the major lipoprotein present, and the relative contents of the different lipid components.

Lp(a) is a lipoprotein rich in cholesterol. It differs from LDL as it contains an additional protein, apolipoprotein (a). Similar to LDL, an Lp(a) particle also contains one molecule of apolipoprotein B.

What Are Normal Blood Levels of Lp(a)?

It as assumed that Lp(a) is produced by liver cells. However, the pathways for the clearance of this substance are not clearly understood.

Plasma levels of Lp(a) rise shortly after birth and the levels appear to become consistent within a few months.

In adults, plasma levels of Lp(a) vary widely, ranging from 0.2 – 250 mg/dL. The levels are similar in men and women.

Studies indicate that about one in five individuals have plasma levels above 50 mg/dL (80th percentile), and about one in four individuals have plasma levels above 32 mg/dL (75th percentile). Lp(a) levels less than 30 mg/dL are considered normal.

The EAS Consensus panel recommends that Lp(a) should be measured in high risk individuals such as those with premature CVD, familial hypercholesterolemia, family history of premature CVD and/or elevated Lp(a), and individuals with recurrent CVD despite statin therapy.

Lp(a) and Risk for Heart Disease

A number of epidemiological evidence indicates that Lp(a) is associated with the risk of CVD.

The Copenhagen City Heart Study found that individuals with plasma Lp(a) levels above 50 mg/L had 2 to 3 – fold increase risk for heart attack (myocardial infarction).

A series of meta-analyses has provided evidence of a link between Lp(a) and CVD.

Studies on patients with familial hypercholesterolemia have provided additional evidence.

Studies have indicated that the association between Lp(a) and CVD is without a threshold, and does not depend on high levels of LDL or non-HDL cholesterol, or the presence of other cardiovascular risk factors. However, some authors have suggested that the risk of elevated Lp(a)is small, if LDL-cholesterol is not elevated.

How Is Lp(a) Involved in Atherosclerosis and Heart Disease?

Lp(a) and LDL penetrate the inner layer of the arterial wall and accumulate together at sites for atherosclerotic plaque formation.

Evidence suggests that Lp(a) may be more strongly retained in the arterial wall than LDL. Furthermore, Lp(a) transports oxidized phospholipids whose plasma levels are strongly correlated with the severity of coronary artery disease. Interestingly, these Lp(a) associated oxidized phospholipids possess pro-inflammatory activity. This might be one of the links between lipids and inflammation in atherosclerosis.

There is also some experimental data suggesting that Lp(a) may promote clot formation in arteries burdened by atherosclerotic plaque. This may be one of the mechanisms behind the involvement of Lp(a) in heart attack and stroke.

How Can Lp(a) Be Modulated?

Lp(a) is mainly genetically determined and therefore refractory to lifestyle intervention.

Dietary changes, exercise and weight loss have not been shown to lower Lp (a).

The data on the effects of statins on Lp(a) are conflicting and the same is true for fibrates. Oestrogen replacement therapy in women has been shown to lower Lp(a), although by less than 10 percent. Other agents that have been reported to slightly lower Lp(a) are aspirin, l-carnitine, ascorbic acid/L-lysine, angiotensin converting enzyme inhibitors, calcium antagonists, androgens and anti-oestrogens.

Fat consumption has not been shown to raise Lp(a). One study documented a lowering of plasma Lp(a) levels in individuals placed on diets rich in saturated fat (a palm oil enriched diet). In keeping with this, other investigators have reported an increase in Lp(a) levels in individuals after they reduced their saturated fat intake. Monounsaturated fats also seem to reduce Lp(a) levels, as shown by a study that reported a significant decrease in Lp(a) levels in individuals whose diets were supplemented with almonds.

Consistent with treatment guidelines, reduction of elevated Lp(a) levels should be a secondary treatment priority, after maximal lowering of LDL-C.

Niacin lowers Lp(a) by approximately 30 percent. Therefore, the EAS Consensus Panel has recommended niacin as the primary treatment for lowering elevated Lp(a) levels. However, these recommendations may have to be reevaluated in light of the results from the recent AIM-HIGH and HPS2-THRIVE trials. These trials did not show any clinical benefits of adding niacin to statin therapy.

Evidence indicates that the new PCSK9 inhibitors that are now being tested in clinical trials may significantly lower Lp(a).


  1. Bill says

    Is it your opinion that Lp(a) is atherogenic? I have heard two opinions. 1. that it is primarily atherogenic & 2. that it is primarily thrombotic. I do have high Lp(a) and am working on reducing mine in the hopes it will mitigate my CVD. Thanks for your discussion on ‘modulating’ Lp(a). I am doing some of what you mentioned and trying a couple of others suggested by my doctor. I was told that it can also he reduced a bit, maybe 10%, by taking DHEA. Have you any input on that possibility. Also I was told high dose EPA/DHA will help but is slow acting and likely will only help if thyroid T3 free & t4 free are near the high side of normal. Mine were both near low normal and am hoping the FO + thyroid will help me get it down. I also take niacin & ascorbic acid.

    • Doc´s opinion says

      Thanks Bill. There is still much we don´t know about the exact role of Lp(a) in the pathogenesis of atherosclerosis and heart disease.Studies have indicated that it may be involved in the atherosclerotic process, where it may possibly play a causative role. Other studies have indicated that Lp(a) also plays a role in thrombosis formation, possibly by inhibiting fibrinolysis.

      I am not aware of any studies showing that omega 3 (EPA or DHA) lower levels of Lp(a). However I still believe that omega 3 may have positive effects when it comes to preventing heart disease.

      If Lp(a) is high, the most important thing is to look at cardiovascular risk in general. Although it may be difficult to lower Lp(a) per se, lowering the amount of other atherogenic particles may be helpful. This may be reflected in lowering of LDL-P and ApoB, or their cholesterol surrogates, such as LDL-C. Also, reducing the potential of other risk factors such as high blood pressure, smoking, obesity etc. will be helpful.

  2. Someone says

    Thanks again for the interesting article. I just recently read another article(written by Chris MasterJohn) which was maybe more focused to oxidized LDL and how it contributes to atherosclerosis. Anyways from there I understood that Lp(a) may also play a role in making the LDL particles small and dense. And as I have understood earlier that small and dense LDL particles might be more atherogenic than large LDL particles.

    Article also considers the role of PUFA in oxidized LDL. I would be curious to hear Mie’s and Dave’s opinion on the article since they have been battling on the PUFA subject on earlier post of yours :). (By this Im not trying to restart the long battle you had about RCT etc. , Im just curious how do you see the for example possible atherogenic role of PUFA)

    • Mie says


      when you adjust for confounding factors, sdLDL isn’t really that much more atherogenic than larger LDL. The idea that larger LDL is “neutral” is – simply put – nonsense.

      What comes to oxidized etc etc. LDL; yes, the current view is that harmful modifications of LDL are relevant to CVD, but in clinical sense the benefit can and should still be achieved via reduction in LDL levels, should they be way too high. The higher the LDL level, the more vulnerable your arteries are. It’s not LDL per se, but abnormal levels of it.

      And about pufa: I’ve said all there is for me to say about it in earlier posts. There’s no evidence of current intake levels causing CVD or cancer mortality. Only when intake levels end up being twice as large as e.g. in the USA (from 6,5 –> 12-14) – and in connection with n-3/n-6 imbalance – do problems start to occur. One cherry-picked mechanism (cherry-picked in the sense that n-6 fatty acids have anti-inflammatory properties, too) doesn’t seem to translate into effect in real life.

      And finally: the article by Masterjohn is attacking a partial straw man. Based on the issues mentioned above.

      • Someone says

        Mie, thanks for giving your view on this matter.

        By the way, have you read MastJohn’s arcticle related to Rho ?

        In the article he points out that statins lower cholesterol and inhibits Rho activation through the same mechanism. Rho on the other hand inhibits Nitric Oxide Synthesis.

        I remember earlier having discussion with you about statins and you mentioned that statin’s way to reduce CVD is mainly due it’s ability to lower cholesterol. Your most relevant point was that the more cholesterol is lowered by the statins the better are the results. Now based on MasterJohn’s view, statins ability to lower cholesterol goes hand in hand with it’s ability to inhibit rho activation. Do you think this is totally irrelevant point considering what makes statins effective treating CVD ?
        I was just thinking this since statins has been more effective than other cholesterol lowering drugs. Could the difference be at least partially explained by the statins effects on rho ?

      • Doc´s opinion says

        A number of studies indicate that the anti-inflammatory effects of statins may contribute to their clinical efficacy. The potential mechanisms for these effects are reviewed in this excellent overview; for those who want to dig deeper.

      • Mie says


        the pleiotropic effects of statins do indeed have some added value, but in no way is this comparable to their main effect (HMG-CoA reductase inhibition). Data shows that the clinical value of statins is chiefly related to their LDL-lowering effect:

        To answer your first question briefly: no, I don’t think it’s totally irrelevant. However, there’s no data to suggest that the treatment goal should be changed.

        About the second question: care to define “partially” in terms of %? :-) Bear in mind that statins lower LDL more efficiently than fibrates, niacing etc. etc. See

        Concerning Masterjohn’s article and it’s “take-home” message: the idea that the primary cause of CVD is inflammation is simply not supported by evidence. I’m sure you remember from the previous discussions in which we both have participated that a) e.g. hypercholesterolemia is in itself pro-inflammatory condition and that b) inflammation tends to die out when lipid values become normalized.

  3. Someone says


    but isn’t HMG-CoA reductase inhibition just same mechanism that affects to the Rho activation as well ? So let’s assume(just for fun;) that the Rho would be the one to blame, so wouldn’t the LDL level reduction still correlate with the CVD(because LDL level gets down trough same mechanism) ?

    Anyways, I believe that even if the Rho would be important factor here, LDL level would also contribute to CVD because the more LDL you have in the blood the more likely you probably have more oxLDL as well.

    About MasterJohns comment:
    “the idea that the primary cause of CVD is inflammation is simply not supported by evidence”

    I would rather focus on the actual matter here, instead trying to “resolve” whether MasterJohns views are correct. Anyways, on the other hand when I have been reading his other articles, he might have changed his view a bit. Or at least he thinks that oxLDL is part of the inflammation process, and thus he is not claiming that inflammation would be some mechanism which would not be related to the cholesterol, actually he states on other article:

    “Writers who argue that atherosclerosis has nothing to do with lipids but is all about inflammation and response to injury must contend with the fact that oxidized LDL injures endothelial cells and causes inflammation!”

    @Mie: “About the second question: care to define “partially” in terms of %? ”
    Haven’t really thought about it so precisely :) , Im just trying to understand the whole picture here. Feel free to correct me :)

  4. Someone says

    Hi Doc’s opinion

    My dad underwent CABG 4 months back now we tested the LPA level, it is 40.7 mg/dl. Is it normal ? Also CVD seem to be familial. Any advice/tips Doctor ?

    • Doc´s opinion says

      Lp(A) above 30 mg/dL is generally associated with increased risk. It is important to also look at other lipid parameters as well as other risk factors. CVD has a tendency to run in families. Therefore, if you have a parent or a sibling with CVD, your risk is increased and therefore important to work with the modifiable risk factors.

  5. Ed Thomas says

    I know this site is geared more to health care pros, but I am grappling with a decision and thought I would take a shot at “Doc’s Opinion”. My recent VAP test results: total ldl-c 122, total hdl-c 62, total vdl-c17, total chol 201, triglycerides 71, total apob100 91, lp(a) 23, idl-c 9, real ldl-c 90, real ldl size pattern A, remnant lipo 19, hdl-2 17, hdl-3 45, vldl-3 10. I have had a coronary calcium scan with a reading of 2. I am a 65 yr. old white male, with no other CVD risk factors. Out of what seems to be an abundance of caution, my primary care doc is urging me to go on a daily regimen of Crestor 5 mg. He regards the lp(a) as too high. His reasoning is even if it doesn’t respond to statin therapy, let’s reduce everything else. I am troubled by long term usage and the risk of side effects-as well as cost, and am quite reluctant. I would value your opinion.

    • Doc´s opinion says

      Thanks for the post Ed. The site is geared for everyone, not only healthcare pros.
      Of course I can´t give you any personal advice. What I can say is that statins are not particularly useful when it comes to lowering Lp(a). When giving recommendations on statin therapy I always look at the whole risk profile including family history, smoking, blood pressure etc. If a patient of your age has no such risk factors, a coronary calcium of 2, an LDL-C of 120 and apob less than 100, I would generally not recommend statin therapy.

      • Ed Thomas says

        Thank you very much for your reply. No family history, have not used tobacco of any kind since Feb. 1976, avg bp130/80, stable weight 163 @ 5’7″, 60 mins .aerobic exercise 3-4 x a week, moderate diet and alcohol intake. As I mentioned, my primary care(not a cardio) who I greatly respect and have been going to for very conservative, a self described belt and suspenders guy, is concerned about long term arterial inflammation, stroke factors etc. He dismisses my concerns as to statin side effects, but my concerns are real. At this point, I think I’m just going to follow my gut and decline. Thanks again.

  6. aerobic1 says

    The results from the AIM-HIGH and HPS2-THRIVE trials give rise to the question if elevated Lp(a) levels truly have a cause and effect relationship on the incidence of CVD or if it is just a correlation, and if Lp(a) is really a risk factor that needs to be treated.

    I have battled high Lp(a) for seven years and have tried every imaginable mainstream and alternative therapy and only high-dose niacin has any measurable positive impact on lowering Lp(a) despite treating lipids to ATP III guidelines. I tried high-dose EPA/DHA (6 grams per day) that Bill speaks of above and it also had virtually no impact on lowering Lp(a).

    The negative impact of high-dose niacin is that it consumes SAMe in the methionine methylation cycle and results in elevated homocysteine levels far above normal guidelines. Is elevated homocysteine a fair trade-off for lowering Lp(a)? The only way I can offset the Hcy increasing effect of niacin is to take the methyl donors methyltetrahydrofolate, methylcobalamin and B6.

    • Doc´s opinion says

      You´re absolutely right. There is no proof yet that lowering lipoprotein(a) will bring any clinical benefit. The new PCSK9 inhibitors appear to significantly lower lipoprotein(a) so maybe we will have some more information on this issue when the results of ongoing trials with these drugs have been published.

  7. Richard Shaffner says

    All —

    I found this study fascinating: . Using data from the large WHS, it found that women with a minor allele variant of Apo(a) had much higher Lp(a) levels and a much higher CVD risk. However, that increased risk was eliminated for those that took low-dose aspirin.

    (Interestingly, aspirin had no significant effect on non-carriers of the minor allele, over the 10 years of the study).

    For the individual with high Lp(a), it makes sense to take aspirin, or to get tested for the gene variation, if one is concerned about aspirin side effects. (Berkeley Heartlab has a test; perhaps others do too.)

    For researchers of Lp(a), in light of this study, they should all take aspirin use into account.

    • aerobic1 says

      The trials using low-dose aspirin showed inconsistent results. In one small trial group of 37 CVD patients, low-dose aspirin dropped Lp(a) by an average of 82% ( That was impressive but other trials showed no effect. I believe a person should be tested for aspirin resistance using the AspirinWorks test as a great many people receive little therapeutic effect from aspirin

      The are no double blind RCT trials using aspirin as a therapy for reducing Lp(a) and won’t be either as there is no funding or profit potential for the least expensive therapy on earth. I used low-dose aspirin for 6 years with no noticeable Lp(a) lowering effect. The Pauling vitamin C/lysine/proline produced no beneficial effect for me either.

  8. Richard Shaffner says

    I understand, and I agree.

    It’s worth noting that in the study I referenced, aspirin helped lower Lp(a) in the minor allele “carriers,” but the benefit was greater than those lower numbers would suggest. In other words, aspirin seemed to have a beneficial effect, beyond just lowering the Lp(a) levels. For those subjects, it seemed to eliminate the incremental risk from high Lp(a), in spite of the numbers remaining relatively high.

    So…if one can tolerate aspirin and has those minor alleles, it could be that taking aspirin would reduce or eliminates one’s Lp(a) risk (so to speak).

    Anyway, that’s what I’m hoping…

  9. Shannon says

    Hi my dad passed away suddenly a few years ago whih they belu was heart related. I recently got tests done and found out that my lipoprotein a was 111 (not sure units) they put me on a strict diet and now moniter me every six months they said that if it rises ill have to be put on medication for life. While attempting to explain to me (now 15 years old) what lipoprotein a was, in a bunch of doctor jargon, they mentioned that it cannever be lowered -is that true? And are my lipoprotein a levels dangerous and if so are they life threatening? I would for someone to explain it to me in simple english that I can understand. Thank you in advance.

    • Richard Shaffner says


      I am so sorry for your loss.

      I’m not a doctor. I’m a dad who has lost his wife (and the mother of my children) to cancer. I was very involved in my wife’s medical battle, and I have helped other family members (parents and children) deal with several serious medical issues. So I know a little about dealing with these things from a patient’s perspective.

      I was touched by your note, and if you don’t mind, I’d like to offer the following points and suggestions:

      (1) I applaud your taking responsibility for your own health. You’re getting tests and advice from doctors, as you should. You’re also being curious and wanting to learn more. That is EXACTLY what you should do.
      (2) Your health and medical care are primarily YOUR responsibility. Accepting that responsibility, and managing your own care, will be the most important thing you can do. (It’s fine if others also feel responsible for your care, but you should never let go of that responsibility completely.)
      (3) Medicine and all sciences are ever-evolving. Whatever you hear from doctors now (about tests, diagnoses, prognoses, conclusions, treatments, etc.) will be based on what doctors know and believe now. You can count on that changing over time, even when doctors seem to have definitive answers.
      (4) Sometimes, most doctors will agree about a medical issue and the best course of action. Sometimes they don’t. There are controversies raging now about diets (for example, whether to eat low-fat/high-carb, or low-carb/high-fat). Many doctors are also in raging disagreement about how to test for and treat cholesterol, lipids, and cardio-vascular risk.
      (5) Lp(a) seems to be one of the more important and least-understood factors. So in this case, you might find some doctors who claim to know, others who are guessing, and others who simply say they don’t know what the risk from high Lp(a) is, or what you should do about it.
      (6) (I’ve had Lp(a) readings from 33-66. My doctor used to think I should treat it with niacin. But now, after some recent studies, he’s not so sure. I’m 58, and they may or may not figure this out in time to help me.)
      (7) The good news, for you, is that you’re so young. Time is on your side. Before your risk becomes significant, doctors and researchers should know a whole lot more about Lp(a) and how to treat it.
      (8) It’s understandable why you have asked for clear explanations and definitive answers. There’s nothing wrong with asking those questions. However, I don’t think doctors will have all the answers for you right now. Be patient. They will, probably within the next 5-10 years.
      (9) From what I’ve read, the issue about whether you are at risk from Lp(a), and what should be done about that risk, will depend on your specific genetic make-up. (That’s the future of medicine. They used to treat everyone based on what worked best for most people. In the future, they will treat individuals based on their DNA, and what they expect to work for each individual.) Keep and eye out for those genetic findings, relative to Lp(a) tests and treatments.

      Sorry to go on so long. That’s what I would want to tell you, if you were my daughter. Again, time is on your side. Be patient. Embrace the responsibility for your own long-term health. Keep learning – throughout your life – and you should be fine. And again, I am so sorry for your loss.


      • Doc´s opinion says

        Richard. Nobody could have said it better. I really appreciate your compassionate and rational response. Thanks. More here.

    • aerobic1 says


      Very sorry to learn of your Dad’s passing.

      I find Lp(a) to be a very finicky and unpredictable animal to deal with but you are smart and fortunate to have a doctor who monitors your health. By any lab standard in the US, 111 is a high level whether it be Lp(a) mass or Lp(a) cholesterol. While it is presumed to be an inherited risk factor, Lp(a) has never been clearly shown to cause heart disease.

      Say you have the flu with a fever. The fever is positively correlated with the flu but it did not cause flu. You can take meds to lower your fever but you will still have the flu. Should the fever even be treated?

      Lp(a) could be just a positive correlation with heart disease and not necessarily a cause of heart disease. My feeling is that it is better to err on the side of treating it as a cause of heart disease than ignoring it as just a positive correlation until more is known about it’s significance. Remember, correlation does not necessarily prove causation.

      You may or may not not have to take meds for life. As research evolves, Lp(a) may turn out to be less significant a risk factor than we are led to believe. Just my thoughts.

  10. SC Mishra says

    Test was conducted in reference to back pain and levels are as under,
    Apolipoprotein – A1, Serum 1.3 g/l

    Apolipoprotein – B, Serum 0.81


    My TMT was positive and have undergone angeography in year 2010, no blocked detected. I am taking Atorvastatin 10 mg per day.

    Kindly suggest,
    Thanking You,
    SC Mishra

  11. Casie Williamson says

    I just read what was wrote. Here is whats going on over here. My 11 year old daughter had a TIA on Jan 16,2014 (4 days before her 12th birthday). Dallas Childrens Hospital did a bunch of tests on her and the only thing that came back abnormal were her Lp(a). She was showing 128. She was released from the hospital before we found out her levels. Right now they have her on 2 “baby” asprin a day. Her neurologist informed us that this type of protein was genetic. I went and had mine tested as when I was 19, and pregnant with her, I had a stroke. My level is 143. I am now having my twin sister, mother, and father get their levels tested to see if we can find out more information. Is there anything that i can do to help my daughter? This is so hard for me to understand so I dont even know how to explain this to a now 12 year old. I feel like its my fault that she had a stroke. Is there anything I can do to help her and myself from having bad health issues in the future. Also, I should mention I have Papillary Thyroid Carcinoma with Follicular Variant. Had TT and now with synthroid 175mcg i’m staying around .03 for TSH.

    • Axel F Sigurdsson says

      Thanks for your comment Casie. Sorry to hear about your daughter and I sincerely hope that she will make a full recovery. I’m not a pediatrician and will therefore not be able to help much in your daughter’s case.

      Some studies have shown a correlation between Lp(a) and the risk of stroke. However, we still don’t know whether there is a causative relationship and whether lowering Lp(a) will reduce the risk of future events. As you say, our Lp(a) levels appear to be largely determined by our genes. Lifestyle and diet does not seem to influence Lp(a) very much. Although there are some drugs (like niacins for example) that lower Lp(a) levels in blood, they are not generally recommended because they have not been proven to lower the risk of stroke or other cardiovascular events. The new PCSK9 inhibitors that now are being tested in clinical trials significantly lower Lp(a) levels. However we still not know enough to be able to use these drugs in clinical practice.

      Although high Lp(a) appears to be familial in your case, it does not have to be the only cause of the increased stoke risk that also seems to run in your family. There may be other factors as well.

      Aspirin does reduce the risk of stroke among those at increased risk. Some studies have also shown that it may lower Lp(a). Although lifestyle may not affect Lp(a) very much it certainly affects the risk of new cardiovascular events. So, of course healthy lifestyle and diet choices are important for your daughter. Blood pressure is important as well.

  12. Casie Williamson says

    Thank you for your help with this. I’m going to look more into the clinical trials which you mentioned and see if anything there might be of assistance with a pediatric case.

  13. R.Chandrasekhar says

    R.Chandrasekhar, Bangalore India Dated: 15th March, 2014
    I am Diebetic since 1998. Now as on date, I take Glycomet SR 500 and Becausules cap in the night
    Diapride M 1, Ramitorva cap and ecosprin 75 in the morning after food.
    When I went for regular check this day, the findings were…FBS 136 mg;PPBS 189 mg;Total Chlo 127 mg
    Triglycerides 82 mg;HDL 40 mg; LDL 79.7 mg;VLDL CHlo 7.3 mg;Total HDL ratio 3.18;LDL ratio 1.99;Apoliprotein A 1 124 mg;Apoliprotein B 62 mg; APO B APO A ratio 0,50;High sensitivity CRP 0,02 mg;
    LIPOPROTEIN (a) Immunoturbidometry 51.3 mg….This is the main cause of worry and how to reduce it
    and what are the medications available Please advise the gravity of the situation.

  14. Margo says

    Could you please advise? I am a 51 yr old female, 5’9″, 155 lbs. I am VERY concerned about my LP(a). It is 237 nmol/L. My Apolipoproien B is 91mg. Total cholesterol is 195, HDL 61, Triglycerides 54, LDL 123. I have had chronic achy, heavy, throbbing leg pain for about 15 years now. I also have chronic fatique. My father passed away from a heart attack age 56. I do not know if he had high LP(a). My diet is fairly good, (I know I have to watch my sugar/carb intake!!) and I do exercise. Over the years, I have seen many nutritionists, doctors, and nothing has really helped me that much. I do not want to go on statins, because I have heard it doesn’t really help much anyhow. I have also tried niacin, but once again, it did not really make that big of a difference. Another nutritionist suggested I do a liver cleanse. He is also suggesting I take Nattokinase, Lecithin, and Taurine. I am very concerned about having a stroke or heart attack. Please let me know if there is anything I can do!
    Thank you kindly!

  15. Mahesh shah says

    We have family history have heart deases like my brother has open heart surgery and other brother and sister has angio plast and my parent expired due to heart attack. My wife father also expired due to heart attack.i am 55 years old and I got angioplast and I am regular taking medicine as per DR, advice and my ldl n hdl in control and LIPOPROTEIN is 6.5

    Recently my dr. Has suggest that as you have family history kindly check your kids body check up

    My son whose age is 22 Years old having slim body has lipid profile 170 triglycerides 86 and hdl 45 and ldl 109- vldl 1 7 and choleterol /. Hdl ratio 3. 78 ldl/hdl ratio 2.39 and total lipids 513
    But apolipoprotein a1 is 1.27 apolipoprotein b is 0.94 and LIPOPROTEIN A IS 86 to clear doubt in lab error i have check in other lab and also found LIPOPROTEIN is 64.

    Now advice me whether what thing i have to do to reduce lipoprotein in my son .if requirec which type of medicine i have to start .

    Kindly suggest

  16. Chad says

    I have elevated Lp (a) along with a strong family history of males passing from MI’s in their early to mid 40’s. I made the decision a few years ago to go 100 percent whole foods plant based and avoid all processed foods and oils. I’m following Dr. Esselstyn’s recommendations along with daily running. I began this at age 37 and am now 41. I saw that my Lp (a) did tick up a few points but everything else dropped so much I thought that I was OK. Now, I’m starting to question it from what I’ve seen from low-fat vegan diets raising Lp (a) levels. I’ve asked my cardiologist and she doesn’t seem to concerned. Yet, I’ve had a squeezing sensation in my chest that comes and goes almost on a daily basis for the last year or so. I contributed this to gas or indigestion but eating a plant based diet, I rarely have indigestion. I’m very concerned that I might have done more damage to myself than good. Can you give your thoughts on a plant based lifestyle and Lp (a)? I would hope the studies are referring to processed carbs and not the good whole plant foods that I consume. Thank you.

    • Axel F Sigurdsson says

      Thanks for the comment Chad.
      Generally, Lp(a) is very difficult to modify by diet.
      I don’t believe you’ve done any damage by adopting a plant based diet. In fact such a diet usually affects blood lipids and heart disease risk in a positive way.
      You should absolutely discuss your symptoms, “the squeezing sensation” in the chest with your doctor.

  17. Teri says

    Hi, I’m have been following Esselstyn’s advice that if you can get your LDL C down to 70 or below that you didn’t have to worry about your high Lp a. Is this not true? In addition, I just had NMR LipoPropfile done which showed LDL P 609 and HDL P 42. APO B 74. Lp a remains elevated at 43. I was very excited but now reading your blogs I’m back to feeling frustrated since I have worked so hard to get theses numbers down, albeit with the help of niacin, asa, l carnitine, almonds and Paulings Lysine/proline/Vit C for Lp a. And artichoke extract, and berberine and Zetia for reducing lipoproteins.

    I also was vegan but have added fish oil and fish back into my diet because I learned how important Omega 3s were to prevent CVD and help my Lupus.

    Your imput would be greatly appreciated. Thank you.

  18. amy e wadsworth says

    I am apoe 3/4 and also have an lp a of 75 ..along with elevtaed ldl at 144,..which is no suprise as my apoe3/4 variant causes ovesabsorption of dietary fats and cholesterol. I have tried years of various plans and supplements with varied results. this is so consuming and stressful and still havent found a way to deal with it, the only time my chol and lp a profile was ideal was when i went overboard low fat low carb, lost 25 pounds) which brought me at 80lbs and ended up int the hospital in bad shape. one i reumed a normal diet my chol and lpa shot right up again. it seems there really is nothing other than pure protein i can eat.!.. i really struggle as I never want o be underweight again but the endless stress of my profiles is daunting.
    with apoe 3/4 (causing high ldl) i am told high carb, high plant protein ,low to no animal protein and low overall fat//esp saturated (also read that apoe 4s need saturdated fat bc our brains dont have it readily available and that is why we over absorb it from food..again another contradiction)
    with lp a im told… eat low carb, and high saturated fat, low to no soy and stearic acid (chocolate!)
    with overabsorber of sterols from berkeley heart lab, im told to lower overall intake of plant fats
    each issue contradicts the other.

    if i CANT eat high fat or animcal protein for apoe and i cant eat high carb or plant protein or soy for lp a and then i cant eat high plant fat for sterol overabsoption ..whats left
    im a runner and also a high metabol;ism that needs to maintain about 2300-2500 calories a day.

    do i eat for the apope issue, the lp a issue or the sterol issue. ?

    i need advice!!!
    does it

Let me know what you think!