Lipoprotein(a)

Recent research suggests that blood levels of Lipoprotein(a) or Lp(a) may be an important marker for the risk developing of heart disease. However, measurements of Lp(a) are not widely available and are seldom used in routine clinical practice.

Measurements 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.

Lipoprotein a

Recently measures of lipoprotein particles involved in atherosclerosis, which is the leading 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).

Lp(a) is a strong risk factor for CVD. However, the lack of clinical trial data has 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 with 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. 

advertisement

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, a Lp(a) particle also contains one molecule of apolipoprotein B.

What Is the Normal Range For 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 have plasma levels above 32 mg/dL (75th percentile). Lp(a) levels less than 30 mg/dL are considered normal.

Here’s how Lp(a) lelevls are looked at in terms of risk:

Desirable: < 14 mg/dL (< 35 nmol/l)
Borderline risk: 14 – 30 mg/dL (35 – 75 nmol/l)
High risk: 31 – 50 mg/dL (75 – 125 nmol/l)
Very high risk: > 50 mg/dL (> 125 nmol/l)

According to the Framingham Heart Study, the 90th percentile of Lp(a) levels is 39 mg/dL (1.39 micromo/L) in men and 39.5 mg/dL (1.41 micromo/L) in women (units of mass)

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 elevated Lp(a), and people with recurrent CVD despite statin therapy.

Lp(a) and Risk for Heart Disease

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 meta-analysis of prospective studies provided evidence of a link between Lp(a) and coronary artery disease.

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 firmly 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.

At present, serum Lp(a) concentration does not appear to be significantly altered by realistic dietary changes. Standard dietary intervention such as a low-fat diet has little effect on serum Lp(a) levels.

Currently available data suggests that fat consumption does not 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.

The data on the effects of statins on Lp(a) are conflicting, and the same goes 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-estrogens.

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 have recently been tested in clinical trials may significantly lower Lp(a).

advertisement

100 thoughts on “Lipoprotein(a)”

  1. 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.

    • 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. 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.

    https://www.cholesterol-and-health.com/Does-Cholesterol-Cause-Heart-Disease-Myth.html

    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)

    • Someone,

      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.

      • Mie, thanks for giving your view on this matter.

        By the way, have you read MastJohn’s arcticle related to Rho ?
        (https://www.cholesterol-and-health.com/Rho-Activation.html).

        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 ?

      • 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.

      • Someone,

        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:

        https://www.ncbi.nlm.nih.gov/pubmed/16214597

        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

        https://www.health.harvard.edu/newsweek/Help_for_your_cholesterol_when_the_statins_wont_do.htm

        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.

      • The idea that larger LDL is “neutral” is – simply put – nonsense? This statement is incorrect. Also, simply LDL is not and should not be a precursor to anything wrong, but your total Cholesterol to HDL ratio is important. If your Cholesterol is 300 but your HDL is 95, you are well within normal ranges.

        As for ApoA,
        ApoA and B are both apolipoproteins. Usually, ApoA is associated with HDL (the so-called “good” cholesterol) and ApoB is associated with LDL (the so-called “bad” cholesterol). In actuality they’re both “good.” Lp(a) is an odd fellow that’s kind of a hybrid between LDL and HDL. I don’t actually understand what it’s for. Maybe the busted LDL particles get an A attached to them because the liver is unable to manufacture a new batch of HDL? I’m just guessing wildly here, but the various lipoproteins are actually kind of like address books that tell the lipid particle how to behave (where to deliver their goods). An Lp(a) is kind of schizophrenic because it’s simultaneously an HDL and an LDL particle.

        I don’t think it’s well understood what’s going on there.

  3. Mie,

    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. 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 ?

    • 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. 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.

    • 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.

      • 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 20+yrs.is 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. 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.

    • 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. All —

    I found this study fascinating: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2678922/ . 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.

    • 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% (https://lpi.oregonstate.edu/fw12/lipoprotein.html). 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 https://aspirinworks.com/.

      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. 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. 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.

    • Shannon,

      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.

      Richard

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

    • Shannon:

      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. 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

    LIPOPROTEIN (A) , SERUM 79.8

    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. 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.

    • 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. 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, 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.

    • Hi Chandrasekhar, Hope your Lipo protien (a) levels are normal now. I am having elevated level of Lipo protien(a) problem. Could you provide the medication you have used to lower it and the doctor you had approached please ?
      please send the details to [email protected]
      Satish, HYD

  14. Hello,
    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. 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. 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.

    • 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.

    • Chad, how much good fats are you eating? you should make sure to eat egg yolks, cocunuts oil, olive oil and avocado on a daily basis.

      • Stay away from the olive oils, stick with coconut oils that are medium chain tryglicerides, not long. And do NOT scramble your eggs, this will oxidize the yolk and fats, eat them sunny side up and pull from heat soon as the whites are white. Yolks should be look warm and well below their flash points. If not, don’t bother with the eggs. Keep it all organic brother 🙂

      • Hi Paul. Cooking eggs – interesting comments. Please can you explain the reasoning / what is happening a bit more. Is (soft) hard boiled OK? Appreciated

  17. 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. 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 ..eat 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

    • Amy,

      I’m not a doctor. However, at times I too have had high LDL and high Lp(a). I’d like to share some perspectives as a fellow patient that might help.

      First, let me say that I applaud your doing research and taking an active role in your health. That’s great.

      Second, I think it helps to remember that all the research you see deals with statistics about groups of other people, and at best those statistics can only show correlations. From those correlations, researchers will draw inferences about general tendencies and sometimes even about causality. But when using those findings, one must be careful not to jump to conclusions about what they mean for any specific individual (namely you).

      As an example, almost everyone agrees with the statement that “smoking causes cancer.” But of course that’s too simplistic. Some people smoke and get lung cancer at an early age, in their 20’s. Other people can smoke all their lives, well into their 70’s and 80’s, and never get lung cancer. (They die because of something else.) How can that be, if smoking causes cancer?

      The answer is that smoking seems to cause cancer in some people, because that type of lung cancer is so highly correlated with smoking. (Very few non-smokers get it.)

      So a doctor shouldn’t tell a patient that smoking will give him or her lung cancer. He can’t possibly know that. A doctor also can’t accurately say to a patient that smoking will increase his or her chance of getting lung cancer. No one knows whether it will or not, for any specific individual. (No one knows whether that person might smoke and get lung cancer, or whether they could smoke well into old age and never get it.)

      What the doctor can say, to be more accurate, is: “We know that smokers generally have a much high risk of getting lung cancer than non-smokers. We also know that smokers generally have a much higher risk of having other serious health problems. No one knows whether you would get lung cancer from smoking, or how smoking would affect your health specifically. But since no can know that in advance, we strongly urge all of our patients to not smoke.”

      I think we should apply that logic to all of the factors you mentioned.

      For example, you said that your having an Apo E of 3/4 causes you to over-absorb dietary fats and cholesterol. I don’t mean to be confrontational, but I don’t think you (or anyone) can know that. I too have read studies (and seen Berkeley Heartlab’s material) that makes that inference. The researchers suggest that people with an Apo E of 3/4 tend to have higher cholesterol readings, and they suspect those people tend to absorb sterols (plant and animal) more than other people. But that doesn’t mean they all do, so that might not be what’s happening to you.

      In other words, people with other Apo E alleles can have very high cholesterol, and people with Apo E of 3/4 and 4/4 can have normal and low cholesterol. The same applies to having heart disease. General tendencies are just that. It doesn’t mean those tendencies necessarily apply to you or any other specific individual.

      That logic holds true for every issue you mentioned. Generally, people with high levels of Lp(a) tend to high a higher risk of heart disease. But that doesn’t mean you do, specifically. Many people with low Lp(a) get heart disease, and many people with high Lp(a) never get heart disease.

      That also applies to the various recommendations that you have heard about what to eat. Those recommendations are based on these statistical inferences from observing groups of people, and a lot of guesswork. Even if they are right and those recommendations make sense for a group of people, those recommendations probably don’t apply to everyone in group.

      For example, I saw a recent study that compared three different diets: low-fat, low-carb and low-glycemic. The study used a crossover design, so each participant tried all three diets. As a group, the subjects did best on the low-carb diet. However, when one looked at the results for each individual, it was clear that some people did better eating low-fat, others did better eating low-carb, and some did better on the low-glycemic diet.

      In other words, the key finding of the study was not that the participants generally did best on the low-carb diet. Rather, it was that most of the participants did much better on one of the diets than they did on the others. Therefore, the important lesson for us as individuals is to try different diets and find out which one works best for us.

      In short, you were not among those being studied in any of the research you’ve read. No one yet knows whether those findings will apply to you, or not. Only you (and perhaps your doctors) can figure out how you respond to these factors and what works for you.

      So that’s my main advice. I don’t think you should eat a certain way for a specific issue – sterols or LDL or Lp(a) — based on general tendencies that apply loosely to groups of people. I think we should each try different things, do our own personal research, and eat what’s best for us.

      Now that I’ve said that, there are a few other things you should consider. The LDL reading, which measures LDL-C, is of little help. If you’re really concerned, you could have a test done for LDL-P or ApoB, which measures the number of LDL particles. I understand that is now considered the best single predictor of risk.

      You could also have a calcium scan done, to see how your arteries actually look (you might be worrying for nothing).

      Also, I have read that daily aspirin seems to neutralize the higher risk that some people have from high Lp(a). So if you tolerate it well, you might consider taking a baby aspirin every day.

      Sorry to go on so long. I hope some of that helps. Good luck!

      Richard

      • Hi Richard. A fascinating analysis of the concept of risk which do not get to grips with. You state “For example, I saw a recent study that compared three different diets: ” please can you post the url as I would like to read the detail. Appreciated

      • Robert —

        Thanks. Here’s a link to the article:
        https://jama.jamanetwork.com/article.aspx?articleid=1199154 .
        Note the charts (also attached) that show how each subject did on the three different diets. The individual variations are the real lesson from this study (for us as individuals). It would be absurd to tell everyone to follow the one diet that produced the best average result for all subjects. Clearly the right answer for each subject is a series of individual tests (n=1) to and learn what works best for him or her.

        Here’s another article that makes a similar point: https://ajcn.nutrition.org/content/95/2/506.short
        Richard

      • Sorry! Somehow two charts got combined and added (no clue how I did that). Please ignore the top part of the chart.

      • Hi Richard
        Different subject. Same general topic nutritional research.
        You seem to have been around these sites have good knowledge. I would love to see / look through a table (Excel perhaps?) That lists all the relevant LCHF research on Fats, Sat Fats, Cholesterol and all its sub fractions, and Statins. With columns for the research type (animal, RCT etc) date, who, trial name, number of participants, duration, reference, findings summary etc etc etc. Any ideas that such exists, where found??????
        Thanks Robert

      • Robert,

        I don’t have a Excel list, but I’ve read books and visited websites that refer to many studies. The following might help.

        I think the “Keto Clarity” book by Moore and Westman has a long list of studies, by topic. “Cholesterol Clarity” does too, from a different approach.

        The books by Phinney and Volek are great resources — they refer to many studies and link the findings with their own observations. The book by Gary Taubes are good too.

        Peter Attia’s blog ( https://eatingacademy.com/ ) probably saved my life, or at least made me much healthier. My story is a bit like his, but I’m older and don’t workout at his level. (Who does?)

        Google “pubmed low carbohydrate diet” and other related terms to find studies in peer-review journals.

        Ellen Davis has done us the favor of compiling and linking many findings and studies about ketogenic diets here: https://www.ketogenic-diet-resource.com/

        I hope that helps!
        Richard

      • Well, thank you for providing such a good, informative website and letting us comment on it!

    • Crystal
      I think the best thing you can do at the moment is to teach her the importance of healthy lifestyle. Not smoking, regular exercise and a healthy diet are key issues. Hopefully, in a few years time drugs will be available that can lower Lp(a). This article might be helpful.

  19. thank you so much for taking time to really encourage me not to panic and make the worst conclusion! i really will take your advice to heart. i need to focus less on these issues and enjoy life more. im thinking everything in moderation is the best recipe !

  20. i hv consistenly come across info pointing to
    pufas and carbs raising lpa
    mufa (almond flax ) lowering lpa and ldl
    sat fats lowering lpa. Except the stearic acid component of sat fat ..which is chocolate 🙁
    coconut palm and dairy fat always touted as bad sat fat for ldl. but apparently good for lpa and stearic acid touted as cholesterol neutral is bad for lpa
    so.. whats recommeded for non lpa population is actually opposite of whats rec for lpa population
    my question is :
    with lpa. is it more important to have low ldl ( with still high lpa) or low lpa and possibly higher ldl

    • Amy,

      There are many good questions for which there is no simple answer (or not one that you should believe and take to heart.) I believe that is one of them.

      I suspect the best answer would be, “It depends.” It would depend on many other factors, including how high or low those LDL and Lp (a) levels are, and what one’s other risk factors were. And if you were asking for your own health, it would depend a lot on how you respond to the foods you eat.

      (Who cares how various foods might affect others? You’re not eating for them. All that really matters is how those foods affect you. The bad news is that no research study or blog post will ever answer that question specifically for you. The good news is that we can each do our own experimentation to find out.)

      I have a daughter who just got her doctorate in Nutrition from Harvard. She hates telling people what she studies in social settings (like cocktail parties), because she often gets drawn into heated debates about various diets, and people ask her questions like this one that cannot be answered easily.

      To her credit, my daughter will often end those conversations by saying, “You should eat whatever works best for you.” It’s hard to argue with that.

      Richard

  21. For those patients interested in a non-profit, patient advocacy organization for high Lp(a) please see http://www.lipoproteinafoundation.org. For physicians who would like to help the organization please contact us through our web site, we would love to have your support for more research into Lp(a)! We have some of the world’s leading experts on Lp(a) on our SAB board.

  22. Very very very noteworthy as in a short span of discussion like complicated matter happening inside the cellof the liver & blood stream relating to this topic, only individual liking along with moderate life style based on diet & daily combustion is to be maintained by the side of normal parameter watching that is activity control as well as healthy choice of behavior according to the available data herein Doc’opinion. So nice to see the interaction from all classes of readers is welcome.

  23. Dear All

    I am a 37 Yr Old Male who just got the Results of the Blood Test package I had taken Just as Routine. All the Results came out “WITHIN LIMITS”:
    Total cholesterol, LDL, HDL, Alpo proteins, Triglycerides, Etc
    EXCEPT Lipoprotein (a) which came out to be 99 !!!!

    I have Normal BP, And Underwent a comprehensive Health Check up in April 14 (9 months ago)
    which included ECG, Doppler Heart, NCV, MRI Head, CT Scan Head, Cartoid Doppler and Full Ultrasound of Abdomen….All of which came out normal
    Only I was SEVERLY Deficient in Vitamin D and Moderately Deficient in Vitamin B12
    For which i took supplements and now Levels are Normal

    Only the Lipoprotein Levels have got me Worried Big time

    Pls advice..Thanks in advance

    Ik

  24. hi
    your lp a reading is on the high side as mine is. but taking into account your low ldl and normal readings for all else makes the lp a factor less of an issue. lp a really causes problems coupled with high ldl and other genetic variants such as apoe 4
    i wouldnt worry to much about it.
    possibl reduce carb intake. up the saturated fats ( coconut palm dairy) reduce pufas. increase fish almond flax intake
    i wd speak to your dr about slowly titrate up too 1000 mg niacin and add a baby asprirn

    • Thanks Amy for the Reply

      Its calmed me down a little Bit, I Re Read my reports carefully again and my HDL Value is 42 (Normal should be 35+ as per Report) and my LDL is 130 (Anything less than 130 is Normal, But 130 is Right on Edge)…Rest Everything is More or less NOT at extreme ends of Normal Range

      I will be seeking advice from a Cardiologist tomorrow.

      Is there any Non Invasive Tests which I can Take to make sure my arteries are Healthy and Fine.

      PS: I am naturally quite hyper and get stressed out / anxious easily spl. related to Health.

      Can Anxiety be a cause of High Levels of Lipoproteins ?

  25. one question for us lp a people ! there seems to be correlation btw high endurance athletes and elevated lp a. theory is due to high carb endurance diet and or. appropriate response to constant minor tissue damage

    any thoughts?

    i am an endurance athlete::

  26. hi again. i completly get where you are coming from. i get very overly anxious about health concern i do everything i can to keep healthy. eat clean exercise dont drink smoke go to bed early when i found out about lpa i went over the edge and my extreme response of .. now i really need to reign it in. resulted in huge unhealthy weight loss over exercise and more anxiety and stress on body and bones:: those things were more unhealthy than lpa. and some things we cant completly control. no matter how healthy and extreme i am .. my lpa wont budge. i can only control the way i react .. i have adopted the mind set of if im doing my best to stay healthy then im not going to worry beyond that. i figure it may be my body set point. everyone is different .
    do your best to keep healthy eat moderate carb fat protein exercise and lower stress. adding provens such as almonds flax baby asprin and niacin is reasonable. but beyond that just focus on the other positive parts of you. i have spent way too many hours obsessing over lpa levels and treatments .. my hubby always says its not the cholesterol that will do you in. its the stressing out about it that will

    on an aside. lp a levels are found to be high in the longest living people. ! .

    • Thanks Once again for the Positive Reply. As i have been reading everywhere that LPa Levels are “Genetic” and are not effected by Medicines as such

      But as you rightly pointed out…If Other parameters are in place…its negativity is reduced to a Good extent and worrying will create other issues

      Just for peace of mind, I will consult a cardiologist tomorrow and as per his recommendations take tests to Check the Health of Arteries

      Also I would like to ask you Amy…Do High Values of LPa have any Symptoms ?
      Spl like in your case…Inspite of being Fit and Healthy..the “VALUES” of LPa are High ..Any Specific Symtoms…Or its just a Value On Paper which is so Scary

      Regards

  27. hi

    no symptoms. ive always had high ldl. since teenage years. my hdl remains high btw 80-100 bc i exercise a lot
    i only found out abour lpa six years ago. at times i wish i had never found out
    as theres not a lot to do for it!
    the only symptoms i get are anxiety and panic when i think about it!
    control what you can. exercise diet some supplements and be in the moment not living in :: why me:: or fear of what if:: its destructive mentally and physically
    you could get a calcium score to see if you have any arth. also ask dr to test for particle size of ldl and hdl he ll explain large particles are peotective
    go out. /. watch a movie and let the dr do any worrying if even needed!:)
    stay positive !

    • Thanks

      My All Apolipoprotein levels are also well within limits
      HScrp is also 2.9 (Moderate Risk)
      Calcium 9.2 (Normal)

      All other Ratios of Ld, Vldl, hdl etc all within normal limits

      Basically I had a 75 Point / Parameters Blood Test done as Routine and LPa was a part of it, ALL the 74 Values are Within Normal ranges Except This One !!!!!
      and when I Googled it….It simply Scared me badly….but your posts have been encouraging

      I am planning to get the LPa Retested from another Lab to Rule out any Errors

      and will be talking to a Cardiologist tmrw

      I started taking Amway Nutrilite Multivitamin last month only and will now continue with it and Target a LDL value of 100 (from present 130)

      Wishing you all the best…Thanks for your reply 🙂

      • Dear All

        I retested the LPa levels with another Lab and Result was 120
        (2 days back from a Different Lab was 99)

        As per the Lab technician, such variation could be because of Method used and diff. type of Lab Machinery

        Can anyone shed a Light on this ?

        I am putting down my Cardiac Profile Values:

        Apolipoprotein A1 – 126 (Normal)
        APO B – 87 (Normal)
        APOB /A1 Ratio: 0.7 (Normal)

        HSCrp – 2.97 (Average Risk, but on Higher Side)

        Total Cholestrol – 178 (Normal)
        HDL Direct – 42 (Normal)
        LDL Direct – 131 (Almost Normal-On Edge of being High)
        Triglycerides – 82 (Normal)
        VLDL Cholestrol – 17 (Normal)
        TC / HDL Ratio : 4.2 (Normal)
        LDL / HDL Ratio; 3.2 (Normal)

        My Father and Mother DID NOT have Any CVD History but both have been known to Get Anxious Very Fast (and same with me)

        I am Non Smoker , Non Alcoholic

        37 years Male – No History of BP (Taken BP every 3-4 months randomly and was normal)

        Last ECG Done – April 2014 – Normal

        Last Doppler Echo Heart – April 2014 – Normal

        Last Chest XRay – Apri 2014 – Normal

        Last Cartoid Doppler – April 2014 – Normal

        Last NCV – April 2014 – Normal

        Last MRI And CT Scan Head – April 2014 – Normal

        (These Tests in April 14 were done as a part of Full Body Check up, in which I was SEVEREALY Defincient in Vitamin D (Value- 7)
        and Vitamin B12 (200)

        But AFTER taking Vitamins My recent values were both in Normal Range

        Latest Values

        Vitamin B12 – 490

        Vitamin D – 33

        MY BIGGEST CONCERN REMAINS LP(A) which is around 110 (Average of Both tests)

        I am unable to get an appointment with a Cardio and am very tense

        Todays ReTest has made me more upset (3 days back it was 99 – from a diff. lab….and now its 125…with another lab)

        Please Suggest….If any doctor can give an idea as to whats happening, i will be very grateful

        Thanks

  28. they have different ways to measure some labs use nmol some so use mg i believe
    i would just concentrate on normal range the lab provides you with and go from there

    see if both labs use same measurement parameters..
    your overall provide is stellar!!! lp a is a problem mainly when coupled with other issue such as high LDL small particle size his tri’s etc

    you could boost your HDL a bit with fish oil and niacin (not without direction from dr) as fish oil thins blood and theraputic doses of niacin need to be monitored for liver function effects

    you ARE healthy…the worry will do you more harm.

    • Hello All (Spl. Amy)

      This is the Update, I managed to get appointment from a Experienced Cardiologist

      When I showed him my Reports (Which were All within Normal Range, Except Lipoprotein A….which Showed a Value of 127 in a Repeat Test with a Diff. Lab and Initially was 99)…..He looked at me with a Smile and Asked me….Why Have you come here ???

      Do you have any symptoms Like Shortness of Breath, Pain in Chest, Inability to Climb up stairs, Fatigue, etc

      To which I replied …No

      He asked me “Do you know the No.1 cause of Heart Ailments ? and the Major thing we ask Spl. Heart patients to AVOID “….Its “STRESS”
      And You are exactly Doing that….Taking Stress.

      He said…..No Human Body can Give 100% perfect Results in a Series of Lab Tests.
      But one always has to Climb the Stairs from the Bottom and Not try to Jump straight on Top

      he told me….that a Human Body is designed to Tell if there is a problem….its Just that Humans Ignore it…..try to self diagnose it….or in their busy lives simply Forget about it.

      So the first thing he wanted to ask me…if there was anything which Discomforted me.

      Then he checked my BP and used his stethescope to listen to my heart

      Then he asked me for the “Bottom of Pyramid test reports”….Total Cholestrol, LDL, HDL, Tric,, hscrp and Apo (which luckily were all normal)

      Then he told me…”The Lipoprotein A test which you took by default (as it was a part of package) is NOT EVEN RECOMMENDED to be taken when a General diagnosis is done.

      To that I asked….”WHY ITS SO HIGH THEN”

      Thats when he replied “Its Genes and every human is different….High Lpa in an otherwise healthy person…JUST IS AN INDICATOR…that Genetically…the person has Higher CHANCES of Artery Plaqaue development Due to LDL…Compared to a person who has less value of Lpa ”

      So a Person with High Lpa should Basically Aim at keeping the LDL Value close to 100 and HDL value above 40…with other parameters like Hscrp, Apo, Trig within Normal

      Infact he told me….that Since I am Anxious…lets get it over with….and got me the follwiiing tests done…..ECG, TMT And ECO….which will prove to me that my Heart and Arteried are Healthy…..I got it all done….Which ALL came out to be Normal 🙂

      He just advised me the following

      1. Avoid Stress – Develop a Hobby, Use essential oils, Yoga, etc whatever suits you
      2. Reduce LDL to 100 (which is 130)…which can be easily done by Excercise and avoiding processed food / Junk food . eating out…..Eating HealthyNormal Home cooked meals
      3. Eat 4-5 Raw Garlics everyday (can be split in different meals)
      4. Taking Half Teaspoon of Turmeric Powder in Half a Glass of Milk – Daily Before sleep
      5. At least 2 Ltrs of Normal Temp. water everyday (not more than 1 glass in one go)
      6. Donot fill your stomach 100% in each meal, keep 20% empty
      7. Include Walnuts, almonds, oats in breakfast
      8. Include FIsh in meals and reduce red meat
      9. Take Sufficient Vitamin C
      10. Donot let Vitamin D levels fall below 60-70 (Mine are 30)
      11. Donot let Vitamin B12 levels fall below 500 (Mine were 450)
      12. Eat Slowly taking time to Chew each Bite Properly

      Sorry for such a Long Post…..But I am quite happy with what i learned today

      Wanted to share….Spl. thanks to Amy..who also said similar things in her replies to me

      In a Nutshell…If Everything Else is Fine…and Just One LPa Value is Out….then all one needs to do is to be more careful about his Lifetstyle ..but then Shouldnt everyone be 🙂

      Thank you

      • My oh my ,this is shaman recipe !
        A full load of worn out motherhood statements and a good measure of utter crap 3) and 4). …..what’s missing is rhino horn powder.

  29. hi!! im so happy for you. sometimes all we need is reassurance and you got just that! love your body as long as you take care of it by eating as best as you can exercising and lowering stress :: then you can release yourself from worry. that you are doing the best you can and so much anxiety is due to a fear of lack of control. but i relieved so much anxiety over this issue myself doing the best i can to take care of myself but accepted that beyond that. i wont worry. i am a much happier essy going and less sensitive than i ever have been
    your cardio seems wonderful and introspective and not like many drs to either compound fear or blowing it off.. just remember his expert words if negative thoughts pop in your head and remind youself you have no need to worry!
    enjoy your oatmeal with almonds take your vit d3 and b12 eat fish practice some yoga and breathe….i do eat lots of raw garlic !! hopefully you have people around you that have a weak sense of smell:)

  30. Just my humble opinion, but you can’t let the stress of the fear of the numbers add to any potential problems you may or may not have. Every day you do that, you’re diminishing your quality of life for the days of health that you DO have. I say that with all due respect because I am quick to focus on these things and have had to learn to deal with them for the last 36 years.

    My dad’s dad died of heart attack #3 at age 56 when I was just a baby. Bypass surgery was in its infancy and not common like it is today. My dad had a heart attack at 42 when I was 12 years old (I’m now 48). He had 4 bypasses at 46 and then about 3-4 years ago at 74 he had another double-bypass surgery. All of his native arteries and the bypasses had shut down except for one, and it was pretty junked up. He had no further heart damage as he was running off of collateral circulation and the junky bypass. From the point of dad’s first heart attack, my mom went into hyper-vigilant mode and I was paranoid about every bite of food I put in my mouth. But I had to eventually come to the realization that I could only do what I could do, and the rest I’d have to leave up to fate, God, or whatever you believe in.

    My dad’s cardiologist had my blood tested and my cholesterol was high, so in my 20’s I started on Mevacor. I’ve been on Mevacor, Zocor, Lipitor, and now Crestor. I’ve been on about ever cor and tor there is. I also took Questran for a while…for those of you who remember, that was that nasty powder drink that was like drinking cement and it was supposed to bind cholesterol in the colon.

    Fast forward several years. My brother had a heart attack at 39 and then 4 bypasses at 40. I was 36 at the time. And then in 2012 it was my turn. I had a heart attack at 47 years of age (interestingly enough, in the exact same place of the heart that my dad’s was). They treated it with meds as I was a borderline surgery candidate. I had many blockages throughout my heart, but they didn’t want to operate too soon as the grafts wouldn’t “take” as well if it was pre-mature. Well, 8 months later I had another heart attack (a minor one, if you can call it that) and ended up with 6 bypasses at age 48. Keep in mind that all this time, I’ve been on statin therapy and seen a cardiologist since I was about 20. I always watched my diet the best I could (but could have done better, I’m sure).

    Now I’m under the care of 2 cardiologists, one of which is a board certified lipidologist. He had the major tests run and my LP(a) numbers are off the charts. My concentration of LP(a) is 225+ and the number of particles came in at 585. A fabulous combination. 🙁 Am I freaking out? Yeah, in some ways I am. But we have a process we’ll follow. I’m currently on aspirin, plavix, crestor, metoprolol, zetia, and 1g of niacin a day. I’m supposed to double the Niacin in about 2 months. In about 9 months, we’ll test again and see where things land, and if it’s still sky high, my lipidologist wants to consider trying the PCSK9 drugs if and when they finally hit the street. I’m not keen on feeling like a guinea pig, but at the same time, I’m feeling like if I were to look in Webster’s dictionary at “coronary artery disease,” I’d see a snapshot of my family. I stayed in cardiac rehab on the maintenance program, so I’m getting plenty of exercise (not that it helps with the LP(a) but I figure it has to help all the other factors). My family also has difficulty raising the HDL numbers, too, so that’s an issue.

    I know if it’s still determined that LP(a) is a smoking gun for what’s going on in my family that I can undergo LP(a) apheresis, but it’s not something I want to do or look forward to. At the same time, it seems like cardiology has come a long way since my dad’s heart attack, and the more we learn, the more we can treat. Will we find out tomorrow that what we thought today wasn’t quite right? Maybe. But it’s always like that and I’ve come to the conclusion that the practice of medicine is in some ways like gambling. Based on what we know today, what are the greatest risks and how do you manage them. You might be trading one risk for another, but we all have to make those calls with our doctors.

    Not sure how to take care of my diet at this point. I need to keep the “normal” factors under control while most things say that a low-fat diet might increase the LP(a). Go figure. Anyway, that’s my story. Sorry so long…the whole LP(a) thing is new to me, and I’m learning as I go. But for those of you who are stressing yourselves to the point of making yourselves sick over it, STOP! (I know, easier said than done). After my surgery, I had about 3 months on the couch and taking short walks that put some things in perspective. None of us knows how many days we have left. I could get my LP(a) down to minute levels and then get hit by a bus. So live today and do today the things that make your heart sing and the things you find important. Monitor your health, but don’t let it become an obsession to the point that it takes away from a good life to be lived.

    Pardon me while I step off my soapbox. 🙂 Wishing you all the best in health and in life.

    • Dear Michael

      Thanks so much for sharing your story. I think every cardiologist knows how difficult it is to deal with a family history like yours. I hope the new PCSK9 inhibitors will be a game changer for people who are at high risk, and they certainly do seem to lower Lp(a) more than any other intervention known to us.

      It does appear that you are in good hands with two cardiologists and one of them a certified lipidologist.

      Of course we can go on and on discussing laboratory variables like Lp(a) and other measures of risk. But we’re all humans and there’s only one end to our sometimes complicated lifes.

      Therefore I think your most important message is, as you so elegantly put it:

      “So live today and do today the things that make your heart sing and the things you find important. Monitor your health, but don’t let it become an obsession to the point that it takes away from a good life to be lived”.

      I highly appreciate your thoughtful and well written input and wish you all the best.

  31. This is a super-informative link. Thank you! I am somewhat concerned from my recent labs… but I need to know just how concerned I should be…?

    The good news: HDL68; LDL Density Pattern: A; ApoB 99; Triglycerides 71…

    The bad news: Total LDL 138; Total Cholesterol 223; Lp(a) 22…

    Most other numbers from my VAP are in the desirable ranges…

    I am working hard (but trying to lower stress at the same time 😉 ) at lowering my LDL (with a more plant-based diet; oatmeal; losing 10 extra pounds). I exercise moderately/regularly and really value total, holistic health. How concerned and vigilant should I be? What other suggestions (natural supplements) would be recommended?

    Thank you so much! 🙂
    Scot

  32. hi..my numbers are very similiar to yours..but my lpa is evenn higher at 35 I eat very clean am vigilant about exercise and try my best to be mindful and keep stress at bay. Though my habits are better than those of probably percent of the population, I have always battled high LDL. *( btw your HDLs are great and are a negative risk factor) The concern with lpa is that not much other than niacin really helps so diet exercise dont affect it much lp a coupled with higher LDL is when it becomes a problem. That being said, normal LDL levels USED to be set at 140 or below..so really your LDL are only borderline. I would continue a more plant based diet (though SOY has been shown to increase Lpa but lower LDL) and concentrate on the LDL numbers Three supplements I would advise are a good quality D3 vitamin, a fast release Niacin working up to 1000 mg at night as that is when cholesterol synthesis happens and tall tree phytostanol capsules (google on line) to take with every meal
    you may want to check out your APOE status apoe 3m and 4s are both very sensitive to cholesterol and dietary fat and tend to overabsorb both with lower than average clearance. markers include high LDL..if you show to be 3 or 4 apoe limiting dietary fat esp saturated is the protocol as is a more plant based/fish/lean protein plan

  33. Based on what I read here, I should be dead!

    I am a 59 year old woman trying to find a cardiologist who understands the risks of elevated lp(a).

    Both grandfathers, my father and my brother all died of widow-maker heart attacks at a young age. (My brother, at 52, was the oldest by 6 years.) Despite a healthy diet, reasonable weight (5’5″, 120 lbs.), and a consistent exercise habit (have walked 1200 miles a year for the last 7 years, practice yoga 2-3x/week), my LDL-C levels have crept up over the last several years. My GP ordered an lp(a) test in 2013 for the first time last year to see if statins were in order. The results came in at a mind-boggling 1060, and the lab report indicated that “Results were verified by repeat testing.” He ordered a heart CT scan, which came back with a calcium score of 357 (90th pctl) and showed calcification of the aortic valve. He referred me to a high;y respected cardiologist, who dismissed all my concerns after performing an echo cardiogram that showed that the valve, though “mildly thickened”, showed “good function.” My CRP was only .23. He referred to the Framington study, and said that my BP(avg. 110/70), cholesterol levels, CRP, and lack of any physical symptoms all suggested that I did not need to go on statins. Frankly, this was exactly what I wanted to hear, so I put my fears behind me and stayed off statins. There were few dietary or exercise changes I could make, so I continued my life pretty much as before. (I am a 7-year lung cancer survivor: I learned many years ago how to live with the ever-present threat of death, and odds that don’t look good.)

    This year my labs showed: Total cholesterol of 248, with LDL-C 139, HDL-C 96; triglycerides 66; serum calcium 10.3. At my request, we did not retest lp(a), since it seemed unlikely to have changed given what I had read about its life-long stability.

    But there’s a lot more information about LP(a) out there now, and I want to make sure I am doing what I can to mitigate my risk. So, long story, too long (I apologize), what I want to know is:

    1. Can that level of 1060 possibly be right??? Should I request a new test by another lab?

    2. How do I find a doctor who understands LP(a) and will treat/test, etc. appropriately? I believe that based on what I’ve read here and elsewhere I should go on statins and aim for LDL under 100, and I know my GP will happily prescribe accordingly, but I want a doctor who is knowledgeable, not just one who is willing to do whatever I want.

    3. Are there other tests I should undergo to properly assess and treat my risk?

    Thank you for any insights you can offer.

  34. your lpa value is quite high is the value in mg? or nmol? ask to see what normal range is for the lab that tested it
    as far as a dr that knows a lot about lpa (as most DRs don’t even test for it!) opting for a more functional medicine or DO. is a start

    as far as statins go..they are NOT effective for lpa .but will reduce ldl (which helps reduce risk of lpa) so the avenue you need to explore is it more important to reduce LDL to lessen risk of high lpa or aim to reduce lpa (thru high vit c /lysine/proline doses) niacin, check out heart technology powder.

    I take niacin at 1000 mg it is the ONLY med that’s proven to lower lpa and ldl and raise hdl however it is NOT risk free. As a middle aged woman you should consider BIO Identitical progesterone/estrogen cream ..from a compounded pharmacy. it has been proven to lower in women 10 percent range

    diet and exercise decrease all other risks but don’t really affect lpa ..though strangely saturated dairy fat has been shown to lower values and surprisingly SOY raises it. almonds and flax lower it

    CRP , Homosystine and Vit D are all important to test You could find a dr that does the Berkely Heart Lab chol panel its very thorough. as there are other components of chol that are important. also your apoe status reveals a lot..apoe 4 genes overabsorb and don’t secrete fat and cholesterol well. if you do have apoe4 low fat diet is prudent. (opt for some dairy fat instead of vegetable oil fat)

    in hunter gatherer times LPA was a benefit to have in survival/starvation. so lpa may not be so bad its lpa coupled with inflammation that is the problem.. inflammation from processed carbs sugar fatty fried food

    find a natural focused dr. get Berkeley lab test done, possible start on immediate release niacin and look into the heart technology , limit soy add some full fat natural dairy like grass fed butter or milk or yogurt, cut back on vegetable oils except olive and macadamia, one serving of whole almonds and / or flax daily, exercise and sleep well

  35. Why does steric acid have beneficial effect on LDL but raises lp-a.
    So in light of high lp-a is it more important to focus on foods that lower LDL but raise Lp a. Like stearin acid , unsaturated fats, non fat dairy and chocolate or concentrate on foods that lower lp a but may raise LDL such as high fat dairy coconut oil fatty meats

    It’s a dietary mess

  36. Pingback: Doc's Opinion
  37. i know lpa has both an apo b and an apo a attached. my apo A1 levels are high and my apo b levels are loq both of which considered desirable but since i have high super high lpa (135 mnol/dl) could it be hte (good)apo A1 levels are high b/c i have high lpa
    or perhaps having high apo A1 level are good to have if one has high lpa ? anyone have insight also, I know SAT fat can lower lpa and carbs and unsaturated fats can raise lpa (though the reverse is true for lowering ldl–so which is more prudent lowering ldl or lowering lpa)? anyways, stearic acid is a sat fat but i have read several studies showing its the single SAT fat that raises lpa and that is a major concern on mine not bc i eat a ton of meat or dairy but I consume a HUGE amount of /whats considered heart healthy dark chocolate. which is incredibly high in stearic acid (saturated fat)

Leave a Comment

This site uses Akismet to reduce spam. Learn how your comment data is processed.

Tweet
Pin20
Share186
Share2