Lipoprotein(a) Research Foundation

There is no longer any doubt that lipoprotein(a) is a major causal factor in heart disease:

Meta-analysis (combined re-analysis) of 27 prospective studies:
Danesh J et al. Lipoprotein(a) and Coronary Heart Disease: Meta-Analysis of Prospective Studies


Lp(a) and "subclinical" atherosclerosis
Brown SA et al. The relation of lipoprotein[a] concentrations and apolipoprotein[a] phenotypes with asymptomatic atherosclerosis in subjects of the Atherosclerosis Risk in Communities (ARIC) Study.

Lp(a) and oxidized LDL
Tsimikas S et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease.

Lp(a) predicts peripheral vascular disease
Valentine RJ et al. Lp(a) lipoprotein is an independent, discriminating risk factor for premature peripheral atherosclerosis among white men.

Peltier M et al.Elevated serum lipoprotein(a) level is an independent marker of severity of thoracic aortic atherosclerosis.


Lp(a) across various populations
Gambhir JK et al. Association between lipoprotein(a) levels, apo(a) isoforms and family history of premature CAD in young Asian Indians.

Weber M et al. Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians.



Lp(a) and stroke risk
Jurgens G et al. Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease.

Willeit J et al. Lipoprotein(a) and asymptomatic carotid artery disease. Evidence of a prominent role in the evolution of advanced carotid plaques: the Bruneck Study.




From just about any direction, Lp(a) has been conclusively associated with atherosclerotic disease. We have more than enough data proving association.

But there are two areas of desperate need:

1) Data on effective treatments.

2) Raising awareness of this widely unknown (among the public) and ignored (among health professionals) genetic condition.

Treatment remains a real struggle. In a recent detailed Track Your Plaque Special Report, Unique Treatment Strategies for Lipoprotein(a) Reduction, we summarized the treatment approaches that have some power to reduce Lp(a) and/or its potential for causing heart disease. But, even armed with an appreciation for the world's scientific literature on this genetic condition, full control remains difficult for many people.

Track Your Plaque's HeartHawk has Lp(a) and he has struggled with this pattern for the last several years. He details some of his thoughts in a recent blog post.

More research and clinical studies are required and we need it soon if we hope to gain better control over this genetic pattern that affects up to 20% of people with coronary or vascular disease. Much of the needed research is sophisticated, background work similar to that being done by Dr. Santico Marcovina at University of Washington, Dr. Angelo Scanu at the University of Chicago, and Dr. Sally McCormick in New Zealand.

However, much of the needed research also consists of brief clinical experiences that detail whether or not there is an effect of various potential agents. Larger experiences, for instance, with potential treatment agents such as various phospholipid fractions, acetylcysteine, antibiotic regimens, some hormonal treatments, etc. could be performed quickly and simply. These studies would not require the $20 or $30 million typically spent by a drug company for a study, nor the several hundred million dollars to gain FDA approval of a new agent. They would simply be examinations of existing agents. These studies still cost money, require expertise, staff, and equipment. But the cost is a tiny fraction of the drug industry's investment in research. But it also means that investment return is nil from a drug manufacturer's perspective. Yet there are literally dozens, perhaps hundreds, of agents that hold some promise but have not been thoroughly studied.

For instance, if a specific modification of the phosphatidylcholine molecule were to generate a substantial Lp(a) reducing effect, Merck, Pfizer, and AstraZeneca would yawn--it is non-patent protectable, cannot be protected from competitors through the costly FDA approval process, and therefore is simply not worth their investment--regardless of whether it works or not.

(This is yet another example of how the drug industry, as well as hospitals and many health professionals, have lost sight of their real mission: to alleviate disease, not to profit from sickness.)

HeartHawk and I have discussed on a number of occasions whether a Lipoprotein(a) Research Foundation should be formed, an organization that seeks to fund the smaller research efforts that may accelerate productive research in Lp(a) and perhaps yield useful strategies faster than hoping for somebody to simply stumble on a treatment, or wait for the drug industry to create a unique, patentable entity that returns billions.

I'd like to propose that our Track Your Plaque program begin to fund such an effort. But a lot more help will be needed, particularly to generate the money to fund genuine, high-quality research from high-quality researchers.

If any readers of the Heart Scan Blog have any thoughts or insights into this process of creating a foundation, we'd appreciate your input.

Comments (18) -

  • Keyheart

    4/16/2008 1:02:00 PM |

    I am in favor of such a foundation and would be a donor.

  • Anonymous

    4/16/2008 2:21:00 PM |

    I would be more than willing to donate for such a good cause.

  • Anonymous

    4/16/2008 4:28:00 PM |

    As one with high Lp(a), I too, would support this effort.

    Does anyone know anything about an Ultra sound stroke screening test done by a company called Lifeline Screening. They offer 4 tests, one which checks the Carotid artery for blockage, for $139.00.  They have mobile units that travel around and perform these tests and others.

    I had a Heart Scan last year that showed no measurable plaque, but wondered if this type of test was useful for checking other locations of potential plaque?  Or is it hype?  They are going to be in my area in June.

    http://www.lifelinescreening.com/Services/Pages/Index.aspx

    Bonnie

  • Vivian

    4/16/2008 6:20:00 PM |

    I second that

  • Anna

    4/16/2008 9:07:00 PM |

    There is an extra http:/ in the link to HeartHawk's blog.

  • Warren

    4/17/2008 4:16:00 AM |

    I'm a TYP member and would be happy to donate services to set up the organization and obtain 501(c)(3) approval so contributions would be tax deductible.

  • Bad_CRC

    4/17/2008 6:36:00 PM |

    Bonnie,

    Dr. D has said that carotid plaque correlates about 70% with coronary plaque.  CIMT gives you another quantitative measure to track, but one that is a distant second to CAC for longitudinal use (a lot of variation in scores, plus it's deceptively easy to regress).  Still, with the carotid US they can see non-calcified plaque.  I'd think of it not so much as specific for stroke risk as another measure of subclinical, systemic atherosclerosis.  I got one because I'm too young to have calcified plaque; I'm hoping to track that IMT number and thereby avoid ever getting calcification in the first place.  In your situation I'd definitely do it; if I already had scorable coronary plaque then I'd think there's less utility in the CIMT.  Also, it's totally non-invasive -- no radiation.

  • Anonymous

    5/8/2008 7:30:00 PM |

    Just an idea on a cloudy afternoon - TYP might look at coming out with a product line of supplements and apparel to raise funds.  Profits would be dedicated toward a heart health research foundation.  I'm sure TYP followers would appreciate buying supplements that have a TYP quality stamp of approval along with the knowledge that funds generated would be dedicated toward research that helps them. And I've thought it would be fun to show up at a heart walkathon wearing a Track Your Plaque shirt.  A shirt could have a TYP logo on it saying something along the lines of "I trust Track Your Plaque" and then list the  different items that make the program successful.

  • Anonymous

    8/8/2009 7:24:51 PM |

    As a 61 year old women with 7 coronary artery stents, I would be very interested in aiding research and participating in  any studies anywhere. My daughter,a physician just had her Lp(a) tested twice and both times it was 90.My cardiologist has always said my problem was genetic and I am going to ask her to test my Lp(a.Thanks for this site.

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  • Sandra Tremulis

    1/17/2013 8:18:16 PM |

    For those of you still interested in a non-profit foundation for Lp (a)  please contact me serevill@aol.com  I am a survivor and have Lp (a) too.

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Is Lp(a) part of your legacy to your children?

Is Lp(a) part of your legacy to your children?

If you have lipoprotein(a), Lp(a)--the most aggressive known cause of heart disease that no one has heard of--then you need to tell your children.

Lp(a) is a "cleanly" inherited genetic pattern: If either parent has it, there's a 50% chance that you have it. If you have it, then there's a 50% likelihood that each of your children has it. (Note that each child experiences a likelihood of 50%, not 50% of your children. This is because each child is conceived as an independent statistical event. So much for romance!)

The atherogenicity (plaque-causing potential) of Lp(a) also tends to get transmitted. In other words, if your Dad had a heart attack at age 50 due to Lp(a) and you share Lp(a), then you likely share a similar magnitude of risk as your Dad. If your Mom had Lp(a), though passed quietly at age 89 without any overt evidence of heart disease, then you are likely to share the relatively benign form of Lp(a).

For most of us with Lp(a), however, it is best to assume that it has at least some potential for causing heart disease, being the most aggressive cause known. (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.)

At what age should you inform your children? There's no hard-and-fast rule. However, I generally suggest to patients that they talk about Lp(a) with their children when they reach their 20s or 30s, old enough to begin to understand the implications and begin to think about adopting healthier lifestyles. Is treatment required at, say, age 35? That depends on the pattern of Lp(a)-related heart disease in the family: With exceptionally aggressive forms, it might be reasonable to begin treatment at this relatively early age.

Comments (21) -

  • craig&jan

    9/15/2009 4:59:09 AM |

    Finally switched to a new PCP who says she loves lipids!  Very interested in all facets of cardiac risk, thyroid, etc.

    My father is 88 and still very active. My mom passed away at 84 following her first health event which was a stroke.  
    I have been following this blog's recommendations for supplements, diet,etc. The new dr did a lipid panel and without any rx meds, my total was 199, HDL 61, Tri 68, LDL 124.  My Lp(a) was tested by my previous dr and was 34. I was told that was high and I probably had inherited my mother's pattern and she most likely had an Lp(a)problem. The new dr says I must go on Crestor 5mg a day to lower my LDL to 100. She says that will protect me from depositing more plaque in the coming years, in effect immobilizing the Lp(a). Would you say that was a fair assessment and reason to start on a statin?  She feels the lowest dose possible is enough to benefit by lowering the LDL.  Your post is exactly the situation I'm in and adding meds are my biggest question.  I will tell my children who are in their late 20's. I'm in my mid-50's with no other health issues.  I'd love your take on it.

    Thanks.

    Jan

  • craig&jan

    9/15/2009 4:59:09 AM |

    Finally switched to a new PCP who says she loves lipids!  Very interested in all facets of cardiac risk, thyroid, etc.

    My father is 88 and still very active. My mom passed away at 84 following her first health event which was a stroke.  
    I have been following this blog's recommendations for supplements, diet,etc. The new dr did a lipid panel and without any rx meds, my total was 199, HDL 61, Tri 68, LDL 124.  My Lp(a) was tested by my previous dr and was 34. I was told that was high and I probably had inherited my mother's pattern and she most likely had an Lp(a)problem. The new dr says I must go on Crestor 5mg a day to lower my LDL to 100. She says that will protect me from depositing more plaque in the coming years, in effect immobilizing the Lp(a). Would you say that was a fair assessment and reason to start on a statin?  She feels the lowest dose possible is enough to benefit by lowering the LDL.  Your post is exactly the situation I'm in and adding meds are my biggest question.  I will tell my children who are in their late 20's. I'm in my mid-50's with no other health issues.  I'd love your take on it.

    Thanks.

    Jan

  • Dr. William Davis

    9/15/2009 11:57:55 AM |

    Hi, Jan--

    Sadly, that is the typical primary care response, someone who has minimal to no insight into Lp(a).

    So, no, I would not agree with this approach that was first popularized by a single substudy performed by Dr. Greg Brown at the University of Washington.

    I take a very different view of Lp(a) that varies depending on age. However, this is a lengthy topic either for a future post or refer to the detailed discussions in the Track Your Plaque website.

  • ABick

    9/15/2009 3:47:10 PM |

    Dr. Davis - Is any amount of Lp(a) a significant risk factor for CVD?  Or is there a relatively safe threshold that if one is below there should be limited risk?

  • steve

    9/15/2009 4:42:52 PM |

    Dr Davis:  what would you say is a high Lp(a)? The NMR range is <75nmol, and the other measurement i think is <32or 40dl.  Would a 30-40 be high on NMR, or 15-20 per dl?
    Thanks,

  • Scott Miller

    9/15/2009 8:01:37 PM |

    Dr. Davis,

    I read all of your posts, greatly admire your practice, open-mindedness, and vast knowledge.

    I have measured my Lp(a) for several years, and have kept it at a bare minimum, usually below 8, most recent a reading of 3. I do this through a paleo-like diet:

    o High-fat (avoiding polyunsaturated fats, but high in saturated fats, mono unsaturated fats, and marine omega-3's)
    o Moderate protein (mostly from animal sources)
    o Low-carb (no grains, no added sugars, absolutely no processed fructose, and eating mostly high-water-volume vegetables, which are naturally very low in actual glucose polymers)

    My primary goals:
    o Maintain ultra low inflammation
    o Maintain low insulin usage (thru maintaining low-normal blood glucose, in the 80's)

    I'm 48, in supremely great health, and look around 35-yrs-old.

    My question: I've thoroughly looked for studies linking Lp(a) to gluten consumption, but I've come up empty. Are you aware of any studies?

  • Dr. William Davis

    9/15/2009 9:17:14 PM |

    AB and Steve--

    Because there are several different methods to measure Lp(a) for which the "reference ranges" differ, it is best to consult the range offered by the lab used, which are pretty good indicators of normal vs. abnormal.

    Scott--

    I know of no data specifically relating gluten to Lp(a). Anecdotally, there may be an effect, but it is likely relatively small.

  • Scott Miller

    9/16/2009 2:14:38 AM |

    Dr. Davis, I thought you had found in your practice a link between gluten and Lp(a). Or, at least, wheat and Lp(a)?

  • Dr. William Davis

    9/16/2009 2:30:01 AM |

    Hi, Scott-

    It's difficult to separate out the effects of wheat elimination vs. carbohydrate reduction, increased fat/oil intake. So I cannot say with absolute confidence that gluten specifically affects Lp(a).

    It's an interesting concept, but I don't believe that we have an answer.

  • David

    9/16/2009 4:41:08 AM |

    Dr. Davis- Have you ever seen Lp(a) cause heart disease in the very young? Under 35 or even under 30? I know that even children can have high Lp(a), and it makes me wonder if plaque growth is going on throughout childhood in these cases or if it is rather somehow "activated" once a certain point is reached and accelerates in a very short time toward the kind of events we see in the 40s and 50s age groups.

  • Lou

    9/16/2009 4:16:09 PM |

    Dr Davis

    I found a lab in Europe that will do an Lp(a) test and also Apolipoprotein A. I want to do the Lp(a) test as you suggest.

    The lab also offers an Apolipoprotein B test. Is the Apolipoprotein B of any use value? I couldn't see much info about it on your blog/book.

    Thanks
    Lou

  • Kent

    9/16/2009 4:54:47 PM |

    I see various thoughts and studies on the effects of monounsaturated fats on LP(a). I see Scotts example of using lots of saturated and monounsaturated fats and lowering his LP(a). I see other studies where they say monounsaturateds can raise LP(a) by 10-12%. What gives?

  • Dr. William Davis

    9/17/2009 1:45:11 AM |

    Hi, David--

    Rarely will Lp(a) cause heart disease before age 35. There are always exceptions, but they are exceptionally rare.


    Lou--

    Apo B is an improvement over calculated LDL. Yes, it is worth the few extra bucks. My personal favorite, however, is NMR LDL particle number, the best measure of LDl by a long stretch. Apo B is a second best.

  • Dr. B G

    9/17/2009 2:13:23 PM |

    Kent,

    Saturated fatty acids (SFA)indeed potently control Lp(a) in the clinical trials as well as anecdotally in our TYP membership. Why? SFA are actually hormonal in action, binders of receptors just like omega-3 fatty acids which lower inflammation and raise HDLs.

    There is a study that shows if Lp(a) is = or < than HDL2, Lp(a) is effectively 'neutralized'. Some of our members had HDL2 of > 40-50 mg/dl. In fact, Lp(a) and HDL track  together and  Dr. Davis' TYP program includes every facet and strategy that raises HDL to one's genetic potential:
    --thyroid and hormone replacement
    --wheat/gluten/carb elimination
    --vitamin D

    With every 10% increase in vit D, there is a ~1% increase in HDL. Did u know Crestor raises vit D by 159%?! Of course Crestor has NASTY side effects -- Crestor raises oxLDL + Lp(a)).

    -G

  • Dr. B G

    9/17/2009 2:13:23 PM |

    Kent,

    Saturated fatty acids (SFA)indeed potently control Lp(a) in the clinical trials as well as anecdotally in our TYP membership. Why? SFA are actually hormonal in action, binders of receptors just like omega-3 fatty acids which lower inflammation and raise HDLs.

    There is a study that shows if Lp(a) is = or < than HDL2, Lp(a) is effectively 'neutralized'. Some of our members had HDL2 of > 40-50 mg/dl. In fact, Lp(a) and HDL track  together and  Dr. Davis' TYP program includes every facet and strategy that raises HDL to one's genetic potential:
    --thyroid and hormone replacement
    --wheat/gluten/carb elimination
    --vitamin D

    With every 10% increase in vit D, there is a ~1% increase in HDL. Did u know Crestor raises vit D by 159%?! Of course Crestor has NASTY side effects -- Crestor raises oxLDL + Lp(a)).

    -G

  • Anonymous

    9/17/2009 6:32:59 PM |

    My brother had a MI right after he turned 29. My parents now in sixties, do not have cholesterol related heart disease yet although my mom has some issues now due to thyroid problems. She has also developed diabetes unfortunately.

    Would this be Lp(a) related incidence?

  • Kent

    9/18/2009 5:10:58 PM |

    Dr. BG, Thanks for your response on the subject of fats. I was aware that saturated fats could substatially lower LP(a), however my area of concern has more to do with the mono unsaturated fats. Scott mentioned how he had lowered his LP(a) with a diet that included high intake of the mono unsaturated fats. Yet, I have read elsewhere that the mono unsaturated fats can raise LP(a) by 10-12%. (Vessby B et al 2002).
    So I guess my question remains do monos raise or lower LP(a)

  • Florida Butterfly

    2/9/2010 2:07:29 AM |

    I am 22 and just found out that I inherited the elevated lp(a) levels. As of now my number his higher than my dads! He just avoided a heart attack, and had stents put in just before it reached that point. Needless to say I inherited it from him.  I am starting Niacin, only 100 mg.  I will say that it is a serious struggle for me to change my lifestyle as in diet and exercise so early.   My lp(a) # was 65

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    11/4/2010 5:13:10 PM |

    (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.)

  • Anthony Cozzi

    11/24/2011 1:46:27 AM |

    Dear Dr. Davis
    I am 58 years old and have had three stents ( one in 2000 and two in 2008 ).  My Lp(a) is >200 according to my last Berkely Test in 2010.  I am soon having another Berkely Test and would like to know exactly what I should have tested besides my Lp(a) and particle size.  I have been taking Niaspan (1500mg daily) and Simcor 1000/20, Fish Oil and Vitamin D3 ( 6000 iu ) all daily.  Would you suggest me taking any DHEA ?  I would really appreciate hearing from you.  I live in Chicago and could visit your office. 708-925-3010.  Thank you.
    Anthony Cozzi

  • Dr. William Davis

    11/25/2011 2:12:20 PM |

    Hi, Anthony--

    Thyroid assessment is crucial in Lp(a): TSH, free T3, free T4. Also, a DHEA level. Both issues are very important.

    Sorry, but my practice is now closed to new patients, since we were booking 6 months in advance. However, much of this can be found in the Track Your Plaque website.

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