Why haven't you heard about lipoprotein(a)?

Lipoprotein(a), or Lp(a), is the combined product of a low-density lipoprotein (LDL) particle joined with the liver-produced protein, apoprotein(a).

Apoprotein(a)'s characteristics are genetically-determined: If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. You will also share her risk for heart disease and stroke.

When apoprotein(a) joins with LDL, the combined Lp(a) particle is among the most aggressive known causes for coronary and carotid plaque. If apoprotein(a) joins with a small LDL, the Lp(a) particle that results is especially aggressive. This is the pattern I see, for instance, in people who have heart attacks or have high heart scan scores in their 40s or 50s.

Lp(a) is not rare. Estimates of incidence vary from population to population. In the population I see, who often come to me because they have positive heart scan scores or existing coronary disease (in other words, a "skewed" or "selected" population), approximately 30% express substantial blood levels of Lp(a).

Then why haven't you heard about Lp(a)? If it is an aggressive, perhaps the MOST aggressive known cause for heart disease and stroke, why isn't Lp(a)featured in news reports, Oprah, or The Health Channel?

Easy: Because the treatments are nutritional and inexpensive.

The expression of Lp(a), despite being a genetically-programmed characteristic, can be modified; it can be reduced. In fact, of the five people who have reduced their coronary calcium (heart scan) score the most in the Track Your Plaque program, four have Lp(a). While sometimes difficult to gain control over, people with Lp(a) represent some of the biggest success stories in the Track Your Plaque program.

Treatments for Lp(a) include (in order of my current preference):

1) High-dose fish oil--We currently use 6000 mg EPA + DHA per day
2) Niacin
4) Thyroid normalization--especially T3

Hormonal strategies beyond DHEA can exert a small Lp(a)-reducing effect: testosterone for men, estrogens (human, no horse!) for women.

In other words, there is no high-ticket pharmaceutical treatment for Lp(a). All the treatments are either nutritional, like high-dose fish oil, or low-cost generic drugs, like liothyronine (T3) or Armour thyroid.

That is the sad state of affairs in healthcare today: If there is no money to be made by the pharmaceutical industry, then there are no sexy sales representatives to promote a new drug to the gullible practicing physician. Because most education for physicians is provided by the drug industry today, no drug marketing means no awareness of this aggressive cause for heart disease and stroke called Lp(a). (When a drug manufacturer finally releases a prescription agent effective for reducing Lp(a), such as eprotirome, then you'll see TV ads, magazine stories, and TV talk show discussions about the importance of Lp(a). That's how the world works.)

Now you know better.

Comments (26) -

  • Matt Stone

    7/1/2010 4:18:14 PM |

    Ah, thyroid normalization. My favorite. Of course, this has a trickle-down effect on DHEA, estrogen, and testosterone as well. Perhaps Lp(a) is one mechanism by which Broda Barnes was able to prevent heart attacks in his patients?  


  • Anonymous

    7/1/2010 4:39:21 PM |

    Aw darn it. Again health info to be confused about. From Taubes' GCBC I read it was apoB supposed to be the one associated with smaller and denser LDL, "the bad LDL", and I thought apoA was the "large and fluffy" or more benign LDL. I'm pretty sure Dr. Lustig says pretty much the same in his "Sugar, the bitter truth" video. There goes my newly acquired "understanding" out the window again.

  • Anonymous

    7/1/2010 4:42:40 PM |

    The last of the 4 treatments doesnt' seem very specific...

    is "T3" a supplement.. if not, how does one go about normalizing the Thyroid?

  • Mike

    7/1/2010 8:12:19 PM |

    That's a lot of fish oil. I take about 1/5 that amount and would find it irritating to have to increase my intake by a factor of 5.

  • Drs. Cynthia and David

    7/1/2010 9:52:19 PM |

    If the pharma industry could actually come up with drugs that work and don't just chase surrogate markers, I'm sure that would be helpful.  I'm all for nutritional and lifestyle fixes, but this won't work perfectly for everyone all the time, so useful drug therapies would be nice too.

    Anonymous, I think you're confusing LDL pattern A and B ("fluffy" vs dense) with apoA and ApoB (HDL associated vs LDL associated proteins).


  • Anthony

    7/1/2010 10:20:10 PM |

    Dr. Davis,
    How low do you like to see Lp(a)? I've seen recommendations of below 30mg/dl, below 20, and below 10. Mine is 19. Thanks,


  • Dr. William Davis

    7/2/2010 1:12:23 AM |


    Excellent question . . . for which there's no solid answer.

    Despite all we know about Lp(a), no endpoint data have been generated. However, I can tell you that using particle count measurements in nmol/L a level of 60 nmol/L works very well. In mg/dl, a measure of weight per volume, it depends on the method of measurement used. If the "normal" range is 30 mg/dl or less, then aiming for around 20 mg/dl has worked well.

  • Anonymous

    7/2/2010 1:32:33 AM |

    I asked my cardiologist about it (heads up preventive cardiology at a major research institution in Texas) and he said:

    "Well, there's not anything we can do about it, so why test it?"

  • Anonymous

    7/2/2010 1:55:40 AM |

    My cardiologist and PCP have never ever discussed this with me even though I brought it up for discussion. I think my PCP didn't know much and ignored it. I desperately need a new cardiologist (I live in the SF bay area). Anybody here love their cardiologist and like to share some details? I will be forever thankful Smile


  • Paul

    7/2/2010 6:09:32 AM |

    I found this to be a very interesting post over at the Animal Pharm blog concerning this very subject:
    Auto-Tuning Lp(a): Value of Low Carb, High Sat Fat

    They basically come to a very simple conclusion in controlling Lp(a); eat some damn saturated fat! And stay away from the damn carbs!

    Now, let me get back to making my LDL the plain and fluffy kind... someone pass me the ghee please...

  • Harry

    7/2/2010 2:41:24 PM |

    Anonymous and Drs. Cynthia and David, there are several "A" designated particles that frequently get confused. Dr. Davis is talking about lipoprotein(a), with a lower case "a", which consists of an LDL particle with a particle of apolipoprotein(a) attached to it. This apolipoprotein is also designated by a lower case "a". Lp(a) is very atherogenic, and should be minimized.

    Apolipoprotein A, with an upper case "A", on the other hand, is an atheroprotective particle that is a component of HDL. It comes in several varieties. The most plentiful one is designated Apolipoprotein A-I, or Apo A-I, which is the main particle that participates in reverse cholesterol transport, which is the principal way that HDL protects against atherosclerosis, by removing cholesterol from plaque and transporting it back to the liver for disposal. There are also particles designated Apo A-II and Apo A-IV that are also associated with HDL, but their function is not well understood. All the HDL-associated apo A particles are described with the upper case "A".

    Finally, there is the LDL pattern A, which indicates that the LDL particles are mostly large, whereas LDL pattern B indicates that LDL particles are mostly small. These are usually designated with an upper case "A" and "B", and the A pattern is thought to be less atherogenic than the B pattern.

    It is easy to confuse these "A" types, especially Apo A and Apo a, which are two very different particles, the large A apo is good and the small a apo is bad.

  • Kent

    7/2/2010 3:21:25 PM |

    My LP(a) started a year and a half ago at 198 nmol/L, it is now down to 35 nmol/L. Thanks to Dr, Davis's advice that I followed in the Track Your Plaque book, including 4800mg combined EPA, DHA fish oil and 2000mg Niaspan, etc.

    I also want ot mention though that I have been following the Linus Pauling protocol as well, which I believe has a synergistic effect with the other principles applied.

    An interesting thing happened that is worth mentioning, my LP(a) had been gradually dropping over that period of a year and a half from 198 to 45 nmol/L, then I switched to immediate release niacin and my LP(a) jumped back up to 150 nmol/L. That was the only change I made, so I switched back to Niaspan and that is when it went back down to 35 nmol/L.


  • Alfredo E.

    7/2/2010 3:35:40 PM |

    Hi All.The following paragraphs were taken from http://www.drlam.com/opinion/Lp(a).asp

    Lipoprotein A, commonly called Lp(a), is a major independent risk factor for cardiovascular disease. The optimum laboratory level should be under 20 mg/dl and preferably under 14 mg/dl.

    Currently, there is no medicine or drugs that to effectively lower your Lp(a). A high Lp(a) is genetically linked. Fortunately, Mother Nature has provided us a much better non-toxic alternative. It consists of large doses of vitamin C, L-lysine, and L-proline.

    Many conventionally trained physician uses niacin to reduce Lp(a). This does work to a limited extend. Niacin reduces the production of lipoprotein A in the liver, and helps to bring down the lipoprotein A in the blood. This is what most conventional doctors use. However, this approach has its limitations because until the endothelial wall is optimized and cleared, the lipoprotein A level will not be able to reduce significantly. The effects of niacin usually hit a plateau after 6-9 months of therapy. If you are on niacin, make sure the liver enzyme levels are taken periodically to make sure the liver is able to handle the high dose of the niacin.

    This last flower:
    Replacing carbohydrates with proteins ignores the fact that protein, once in the intestinal tract, converts to amino acid. Amino acids increase insulin secretion. It is unclear, however, whether proteins are as potent as carbohydrates in stimulating insulin secretion.

    My comment: Is it possible that protein can produce high insulin secretion? So, what is left for simple humans? No carbs, no protein?

  • Anonymous

    7/2/2010 3:52:13 PM |

    Is the LDL carried in the blood by a protein or has it already been oxidized. I'm trying to understand what form chlorestral is in the blood.

  • David

    7/2/2010 6:17:02 PM |


    It's true that protein stimulates insulin, but the key is that it doesn't only stimulate insulin. Glucagon, insulin's counter-regulatory hormone, is also stimulated. Insulin secretion  is undesirable in the context of low glucagon (which is what we have with high carbohydrate intake), but it's not such a big deal when the ratio of the two are more balanced (which is what we have with low-carb protein intake).


  • Jack C

    7/3/2010 12:03:08 AM |

    The VAP cholesterol profile, which gives the distribution of LDL and HDL particle sizes a other information, shows an upper limit of 10 mg/dl for Lp(a)cholesterol.

    In recent tests, my wife had an Lp(a) of 6 while mine was 8. Through no fault of our own I might ad.

  • Dr. William Davis

    7/3/2010 12:13:49 AM |

    HI, Kent--

    Great results!

    You are living proof that Lp(a) can indeed be tamed. It sometimes requires some unusual strategies, but huge reductions are possible . . . and Lipitor is not part of the equation.

    Long-term commitment to the effort is the key.

  • Anonymous

    7/3/2010 1:29:29 AM |

    what kind of doctor shoudl i see to get the right tests done.  I know I have high Lipo(a) from a previous test at Mayo.  They recommended that I take drugs and I declined.  Now I'm realizing I don't have the complete story.  I need to know more than just my lipo(a) is high.


  • Anonymous

    7/3/2010 6:04:15 AM |

    Are there stats on people with lp(a) that don't develop any plaque?
    Also does the same happen with lp(a) as with ldl? that is that is better to have a higher mg/dl with big paricles than a lower mg/dl with small particles?

  • Hans Keer

    7/3/2010 7:28:36 AM |

    I would say apoprotein(a) is normal phenomenon. What is not normal is the abundance of small dense LDL which apoprotein(a) binds to. So the best way to avoid LP(a), is to avoid the abundance of sugars and starch in the diet. All the other (still costing) treatments for Lp(a) won't be necessary then.

  • jd

    7/3/2010 5:39:38 PM |

    Hi,   I recently had a VAP test done via LEF -- I seem to have some very good numbers and some bad LDL ones.  Any comments would be appreciated.

    all values in mg/dl
    LDL 105
    HDL 71
    VLDL 14
    Total Cholesterol 190
    Triglycerides 51
    LP(a) 4.0
    IDL 3
    HDL2 18
    HDL3  53
    VLDL3 8
    LDL1 PatternA 5.4
    LDL2 PatterA 7.5
    LDL3 PatternB 61.6
    LDL4 PatternB 22.4

    LDL Density pattern = B, flagged abnormal

    Vit D  65.4 ng/ml
    Homocysteine 6.2
    C-Reactive Protein 0.2

    I am 55 yr of age, 6'0", 165 lbs, exercise regularly.

    Heart disease in family, mother's father died of heart attack at 66, other 3 grandparents lived into 90s.  father died leukemia cancer 53, mother living at 80 in good health.  Thanks,   Jim

  • Anonymous

    7/7/2010 4:40:46 PM |

    I use Lugols solution 2% and I have absolutely no idea what dosage I should be using.  I have been using one drop about twice a week, but I would like to have a better idea of proper dosage.  Can you help?

  • James L.

    7/13/2010 9:52:15 PM |

    My cardiologist is treating my high Lp(a) with Niaspan, but even with high doses, it has not had much effect. What do you mean by items 3 and 4 on DHEA and T3? Please be more specific. Thanks.

  • Anonymous

    7/29/2010 9:06:55 PM |

    Could you give some dose for T3 and DHEA that you are recommending?


  • Anonymous

    8/10/2010 8:38:43 AM |

    "If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. "

    Does that mean that high levels of Lp(a) is not inherited from the father?


  • LisaMichelle

    8/24/2011 11:46:03 PM |

    Dear Dr. Davis,

    I'm a 44 yr old female.   I recently had a consultation w/ a cardiologist here in Canada.   I was sent for the consultation because of some strange left jaw and low chest tightness I'd experienced at work the week prior (had been seen then in the ER, normal ECG x 2, normal CXR, normal bloodwork).  Prior to the appt I was told I needed to have fasting bloodwork (so that results were available for the cardiologist to review at my appt).  

    HDL good, LDL good (though at the higher end of the normal range).  Lipoprotein A was 0.55 g/L (which i guess works out to 55 mg/dl which is what the usual unit of measurement is for this one in the U.S.).  The cardiologist told me that all of my bloodwork was normal and that I was very low risk for a heart attack but I requested a copy of my results just to have on file.   I am surprised she didn't mention the elevated Lipoprotein A (normal range for this lab is: 0.00 to 0.33 g/L).   So that got my on my search for info on what exactly Lipoprotein A is, and what it indicates.

    My question is:   I was only told to fast for 12 hours prior to my bloodwork, nothing was said about ensuring I didn't smoke.   Well I did smoke over the 12 hours up until the blood was drawn (even about 30 minutes prior to).   Now I'm reading online that one should not smoke prior to blood being drawn for Lipoprotein A, HDL and LDL, etc.    So could my smoking right up to the time bloodwork done have negatively impacted the results?   Could smoking have made my LDL and Lipoprotein A higher?    Should I have these redone but ensure I don't smoke for 12 hrs prior to blood draw?  (I have a 'quit date' set for next Saturday, so don't worry, I will be quitting).

    Thanks so much,