What tests are MORE important than cholesterol?

In the conventional practice of early heart disease prevention, cholesterol testing takes center stage. Rarely does it go any further, aside from questions about family history and obvious sources of modifiable risk such as smoking and sedentary lifestyle.

So standard practice is to usually look at your LDL cholesterol, the value that is calculated, not measured, then--almost without fail--prescribe a statin drug. While there are indeed useful values in the standard cholesterol panel--HDL cholesterol and triglycerides--they are typically ignored or prompt no specific action.

But a genuine effort at heart disease prevention should go farther than an assessment of calculated LDL cholesterol, as there are many ways that humans develop coronary atherosclerosis. Among the tests to consider in order to craft a truly effect heart disease prevention program are:

--Lipoprotein testing--Rather than using the amount of cholesterol in the various fractions of blood as a crude surrogate for lipoproteins in the bloodstream, why not measure lipoproteins themselves? These techniques have been around for over 20 years, but are simply not part of standard practice.

Lipoprotein testing especially allows you to understand what proportion of LDL particles are the truly unhealthy small LDL particles (that are oxidation- and glycation-prone). It also identifies whether or not you have lipoprotein(a), the heritable factor that confers superior survival capacity in a wild environment ("The Perfect Carnivore"), but makes the holder of this genetic pattern the least tolerant to the modern diet dominated by grains and sugars, devoid of fat and organ meats.

--25-hydroxy vitamin D--The data documenting the health power of vitamin D restoration continue to grow, with benefits on blood sugar and insulin, blood pressure, bone density, protection from winter "blues" (seasonal affective disorder), decrease in falls and fractures, decrease in cancer, decrease in cardiovascular events. I aim to keep 25-hydroxy vitamin D at a level of 60 to 70 ng/ml. This generally requires 4000-8000 units per day in gelcap form, at least for the first 3 or so years, after which there is a decrease in need. Daily supplementation is better than weekly, monthly, or other less-frequent regimens. The D3 (cholecalciferol) form is superior to the non-human D2 (ergocalciferol) form.

--Hemoglobin A1c (HbA1c)--HbA1c represents glycated hemoglobin, i.e., hemoglobin molecules within red blood cells that are irreversibly modified by glucose, or blood sugar. It therefore provides an index of endogenous glycation of all proteins of the body: proteins in the lenses of the eyes that lead to cataracts; proteins in the cartilage of the knees and hips that lead to brittle cartilage and arthritis; proteins in kidney tissue leading to kidney dysfunction.

HbA1c provides an incredibly clear snapshot of health: It reflects the amount of glycation you have been exposed to over the past 90 or so days. We therefore aim for an ideal level: 5.0% or less, the amount of "ambient" glycation that occurs just with living life. We reject the notion that a HbA1c level of 6.0% is acceptable just because you don't "need" diabetes medication, the thinking that drives conventional medical practice.

--RBC Omega-3 Index--The average American consumes very little omega-3 fatty acids, EPA and DHA, such that a typical omega-3 RBC Index, i.e., the proportion of fatty acids in the red blood cell occupied by omega-3 fatty acids, is around 2-3%, a level associated with increased potential for sudden cardiac death (death!). Levels of 6% or greater are associated with reduced potential for sudden cardiac death; 10% or greater are associated with reduced other cardiovascular events.

Evidence therefore suggests that an RBC Omega-3 Index of 10% or greater is desirable, a level generally achieved by obtaining 3000-3600 mg EPA + DHA per day (more or less, depending on the form consumed, an issue for future discussion).

--Thyroid testing (TSH, free T3, free T4)--Even subtle degrees of thyroid dysfunction can double, triple, even quadruple cardiovascular risk. TSH values, for instance, within the previously presumed "normal" range, pose increased risk for cardiovascular death; a TSH level of 4.0 mIU, for instance, is associated with more than double the relative risk of a level of 1.0.

Sad fact: the endocrinology community, not keeping abreast of the concerning issues coming from the toxicological community regarding perchlorates, polyfluorooctanoic acid and other fluorinated hydrocarbons, polybrominated diphenyl ethers (PDBEs), and other thyroid-toxic compounds, tend to ignore these issues, while the public is increasingly exposed to the increased cardiovascular risk of even modest degrees of thyroid dysfunction. Don't commit the same crime of ignorance: Thyroid dysfunction in this age of endocrine disruption can be crucial to cardiovascular and overall health.


All in all, there are a number of common blood tests that are relevant--no, crucial--for achieving heart health. Last on the list: standard cholesterol testing.

Comments (8) -

  • stuart

    5/13/2013 12:56:55 AM |

    Great summary Dr. Davis.  You're the best!

  • Sol y Sombra

    5/13/2013 11:07:44 AM |

    Thank you for the useful information you provide, Dr. Davis. But I have a question: Does it really take 3-4 years to replenish vitamin D stores in the body?

  • Amy Crain

    5/15/2013 2:26:51 AM |

    Dr. Davis..
    My husband decided to give going gluten free a try after I read your book, and shared many things with him.  He has a number of issues.  HBP and taking meds.  Asthma, knee injuries with multiple surgeries over the years, and based on his lipid panel numbers, his dr. like you said, wanted to put him on a chol. reducer.  He went gf for a month, this past month, and just this week had his blood work done.  His LDL # went up from 146 to 164, and his HDL went from 45 to 47.   His Trig at least, dropped from 190 to 122,  So he now has in hand a scrip for atorvastatin (sp.?)..  Even though my husband would be considered a slender 48 year old, he has lost 6 pounds during this month of being wheat free.  I personally began a trek of losing weight a year ago by cutting wheat and sugar, and lost over 30 pounds, going from a size 12 to a 2.  I never had any blood work done, since I didn't have any health issues.  I was really hoping for better results for my husbands numbers so that we could provide a valid testimony to those unbelievers within our family.  I don't have your book memorized, but I've scanned through the blog posts and comments and found bits and pieces about numbers and how some people experience an increase like my husband Bill did.  Could you give me a bullet point laymen's version of the reason for the increase, if it's a concern, and if not, should he get the prescription filled like the dr. ordered so that he can then do the 3 month follow up to see if the med. worked for lowering the #'s?
    OR should I just go back and do some more reading like of the above post and reread the book?
    Thanks!
    Amy

  • Lowering cholesterol diet

    5/17/2013 3:10:25 PM |

    Hey there,

    thanks for the article. I would also like to know does Vitamin C plays any role in lowering cholesterol? I am thinking about writing a blog post about it so thank you in advance dr. Davis.

  • Geoffrey Levens, L.Ac.

    5/17/2013 8:23:48 PM |

    List makes great sense to me but one question arises: In light of recent research showing increased risks outside range of 20–36 ng/ml, do you anticipate any change in your recommendations as to Vitamin D blood level?
    J Clin Endocrinol Metab. Published online March 26, 2013. Abstract

    Thank you.

  • [...] between triglycerides and HDL, those improve with LCHF diet. You can start reading more here;  What tests are MORE important than cholesterol? | Track Your Plaque Blog  Lipid researcher, 98, reports on the causes of heart disease | News Bureau | University of [...]

  • Stephen in Jacksonville

    6/14/2013 9:20:30 PM |

    Tests are important, and I think that there are more people today who are interested in keeping track of their cholesterol levels. This is why I think we live in such a special time. We have access to more information than ever before, and now people can learn about high cholesterol risks without having to go to the doctor. In fact, I have found a number of sites that allow people to track their cholesterol levels online. Obviously, there are some people who may go overboard with access to this information, but I do think that there are plenty of benefits to be had.

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What does "Success" mean in the Track Your Plaque program?

What does "Success" mean in the Track Your Plaque program?

Say you begin with a CT heart scan score of 400.

You correct your lipoprotein pattterns, take fish oil, correct 25-OH-vitamin D3 to 50 ng/ml, correct your other hidden patterns, follow a diet suited to your patterns.

One year later, you get another heart scan. What score would constitute "success"?

With all of our recent talk about record-setting reductions in heart scan scores, is it really necessary to drop your score that much to succeed?

For instance, is our latest record-setting 63% drop in score better than "only" a 10% drop in score? Both represent reversal of coronary plaque. Both signify huge reductions in risk for plaque rupture, or heart attack.

You can read about how we view the various forms of success in the program by reading our latest Track Your Plaque Special Report, Winning Your Personal War with Heart Disease: The Track Your Plaque 5 Stages of Success.

We are making the Report available to everyone. Just go to the www.cureality.com homepage.

Comments (11) -

  • WCCAguy

    10/2/2007 11:22:00 AM |

    Hi Dr. Davis,

    This post touches on a point I've been wondering about.

    You write that a drop in CT heart scan score signifies a "huge reduction in risk for plaque rupture, or heart attack."

    As I understand it, strictly speaking, the score indicates a reduction in the volume of calcium/plaque in the arteries.

    In your books and articles you provide references to the studies which document the statistical correlation between FIXED scores and rupture/heart attack.

    My question is this (and you may have answered this question already elsewhere):  Have there been studies that document a statistically significant relationship between a reduction in plaque volume (as opposed to a fixed value) and risk of a CAD event?

    A follow up question:  Is the actual reason for the risk reduction due to score reduction actually known?  I can imagine that one reason might be that because the arteries have plaque reduced, they are actually larger in terms of blood flow supported than they were before the plaque was reduced.

    My belief, however, is that there could be additional reasons for a reduced plaque over time = less risk correlation.

    Thoughts about this?

    Thanks.

  • Dr. Davis

    10/2/2007 12:13:00 PM |

    Great questions.

    We do know that, if plaque is permitted to grow (by several measures including angiographic studies, carotid ultrasound, as well as heart scan scores), the likelihood of events escalates along with it. This is known with absolute confidence.  

    We also know that reductions in plaque burden are also correlated with reductions in risk, also by just about any measure, though the magnitude of reduction varies, since each approach provides a different persective on plaque composition, all differ on incorporation of the Glagov phenomenon ("remodeling"). More data on event reductions are needed, however. But until recently, genuine bona fide reversal had been elusive.

    Lastly, actual examination of tissue that has regressed is very limited. As you can imagine, if someone asked you, having regressed, to allow a sample of artery tissue to be removed, you'd likely not be interested. Thus, the observations are indirect and come from animal studies and observations like intracoronary ultrasound.

    Actually, reductions in heart scan scores are a surrogate for inactivation of plaque, removal of inflammatory cells, removal of fat-laden tissue, etc. The reduction  in calcium is a parallel phenomenon that we can see. I also wonder, given the wonderful effects of vit D and possibly K2, whether the reduction in calcium provides benefits of its own, independent of the inactivating effects.

  • Anonymous

    10/3/2007 3:56:00 AM |

    While everyone agrees that reduction of atherosclerotic plaque is a good thing, there are several clinical studies that suggest that reduction of calcium in the plaque may not be good. For example, this study found that culprit stenoses in arteries of patients with stable angina had more calcium than those of patients with unstable angina, which had more calcium than those with acute myocardial infarction. This suggests that plaque accumulation in a specific location may actually be beneficial if it stabilizes the plaque and makes it less likely to rupture.

    There is not much data on calcium score reduction because it is so rarely seen. What is needed are long-term studies showing that calcium score reduction does reduce the number of adverse coronary events.

  • Dr. Davis

    10/3/2007 11:53:00 AM |

    I disagree.

    There is a commonly offered argument that calcium stabilizes plaque. I think this is nonsense. There are studies by Renu Virmani and others that demonstrate that the shear and tension forces at the edges of calcified plaque are, in fact, areas of greater stress and thereby risk for plaque rupture.

    While intracoronary ultrasound will sometimes show that a small segment of a recently ruptured plaque will involve a non-calcified segment, we are NOT using calcium in a lesion-specific fashion. We use it as an index of total plaque.

    I also believe that emerging concepts, such as the influence of vitamin D3 on gamma-carboxyglutamic acid Gla protein in vascular tissue are pointing towards the fact that vascular calcification is part of a regulated, active process that influences plaque activity and rupture potential. (See Johnson et al, Vascular calcification: pathobiological mechanisms and clinical implications. Circulation Research 2006 Nov 2006;99(10):1044-59.)

    Increasing calcium scores have been conclusively associated with dramatic increases in coronary events. Likewise, emerging data, including our own, show reducing calcium scores is associated with virtual elimination of events.

    Do you have something better?

  • Anonymous

    10/3/2007 1:53:00 PM |

    No, I don't have anything better - I don't argue that an increasing calcium score is good, only that we have nothing more than anecdotal evidence to show that calcium score reduction is beneficial. And, there are other experts in the field that do not agree that it is. The recent torcetrapib clinical trial shows that not all ways of increasing a generally beneficial lipid such as HDL are theraputic. Have you considered documenting the results of your practice, i.e., what percent of your patients show calcium score change in each of several percentage ranges including reductions, and what their follow-up results are in terms of hard cardiac events? That might stimulate interest in a controlled clinical trial to verify your results.

  • Dr. Davis

    10/3/2007 2:21:00 PM |

    What experts "agree" that a reduction in calcium score is not beneficial? Can you specify who? I know the literature on calcium scoring quite well, and I don't ever recall such a study.

  • WCCAguy

    10/3/2007 9:27:00 PM |

    Dr. Davis,

    The wizard, hmmm, I mean, Dr. Oz says on Oprah that "we'd rather focus on the plaque itself—because the calcium actually might help stabilize the plaque and reduce the chance of it rupturing."

    http://www2.oprah.com/health/yourbody/youdocs/youdocs_faqs_io_10.jhtml

    So, there's the proof you asked for.  It was on the Oprah show.

    And by the way, Oprah's doc says that Ornish has the answer here:

    http://www2.oprah.com/health/yourbody/youdocs/youdocs_faqs_io_11.jhtml

    Seriously, this question of the Calcium Score relationship to risk reduction is a key issue and I appreciate your sharing your knowledge about the question.

    It will be interesting to see if Anonymous gets back to you with expert reference list you've asked for.

  • Anonymous

    10/3/2007 11:05:00 PM |

    I don’t think there is a study that shows that because calcium reduction is so infrequently seen. I have discussed it with the Director of Preventive Cardiology at a State University Hospital who is of the opinion that calcium reduction may not be beneficial. I suspect that most experts would say that there isn’t enough data to conclude that reduction of calcium is either beneficial or detrimental because most have never seen it.

    My point is that several studies show that plaque rupture tends to happen in arteries that have “spotty,” but not extensive calcium, and that coalescence of small calcium deposits into larger deposits reduces the surface area in contact with softer plaque, thereby reducing the extent of the stress risers that can lead to plaque rupture. Quoting from some of these

    “…double helical computerized tomography demonstrates that extensive calcium characterizes the coronary arteries of patients with chronic stable angina, whereas a first AMI [acute myocardial infarction] most often occurs in mildly calcified or noncalcified culprit arteries.” Shemesh et. al., American Journal of Cardiology, 1998 Feb 1;81(3):271-5, Comparison of coronary calcium in stable angina pectoris and in first acute myocardial infarction utilizing double helical computerized tomography.

    “Acute coronary syndromes are associated with a relative lack of calcium in the culprit stenoses compared with stenoses of patients with stable angina.” Joshua A. Beckman et. al., Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1618, Relationship of Clinical Presentation and Calcification of Culprit Coronary Artery Stenoses.

    “The relationship between calcification and clinical events likely relates to mechanical instability introduced by calcified plaque at its interface with softer, noncalcified plaque. In general, as calcification proceeds, interface surface area increases initially, but eventually decreases as plaques coalesce. This phenomenon may account for reports of less calcification in unstable plaque.” Moeen Abedin et. al.,  Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:1161, Vascular Calcification - Mechanisms and Clinical Ramifications.  

    “In AMI patients, the typical pattern was spotty calcification, associated with a fibrofatty plaque and positive remodeling. In ACS [acute coronary syndrome] patients showing negative remodeling, no calcification was the most frequent observation. Conversely, SAP [stable angina pectoris] patients had the highest frequency of extensive calcification…To the best of our knowledge, the present IVUS study is the first to demonstrate the relationship between calcification patterns, arterial remodeling, and the morphology of plaques within the culprit lesion segment. The major finding is that there is a significant difference in the pattern of coronary calcifications at the culprit lesion segment, particularly with respect to size, number, and length of the deposits, among patients with AMI, UAP [unstable angina pectoris], and SAP. Small calcium deposits were significantly more frequent in the culprit lesion segments in ACS than in SAP patients.” Shoichi Ehara, et. al., Circulation. 2004;110:3424-3429, Spotty Calcification Typifies the Culprit Plaque in Patients With Acute Myocardial Infarction.

    Also, there is an MRI study of  the carotid arteries of CAD patients who had been given niacin, lovastatin, and colestipol for 10 years. In comparison with matched, untreated patients, the carotid plaque of the treated patients showed much less lipid but much more calcium than the untreated patients. Xue-Qiao Zhao, Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1623, Effects of Prolonged Intensive Lipid-Lowering Therapy on the Characteristics of Carotid Atherosclerotic Plaques In Vivo by MRI.

    It seems that reduction of the “spotty” calcium may reduce the likelihood of plaque rupture, but reduction of coalesced calcium such as is seen in stable angina patients may  increase the surface area of calcium (if the coalesced calcium reverts to spotty deposits) and therefore be detrimental. From the standpoint of evidence-based medicine, the only way to be sure of the effects of calcium reduction is to conduct a clinical trial of patients undergoing such reduction.

    In the meantime, Dr. Davis, since you are one of the few cardiologists whose patients are experiencing calcium score reduction, it would be of great benefit if you would document the results of your practice in a quantitative way.

  • Dr. Davis

    10/4/2007 12:30:00 AM |

    I believe that you are confusing two phenomena.  

    Tissue characterization of specific plaque locations that are prone to rupture (or have ruptured) examined by techniques such as intracoronary ultrasound, is distinct from the concept of using coronary calcium scoring as a surrogate measure of total plaque volume.

    I believe that lipid-laden, calcium-poor plaques do tend to identify sites more prone to rupture. I have witnessed this myself in many intracoronary ultrasound procedures personally performed.

    This is different from using calcium as an index of plaque. While we are uncertain of the relationship of calcium to total plaque in people who have experienced calcium score reduction, all circumstantial evidence points towards dramatic regression of lipid laden plaque, regression of inflammatory cell composition, replacement by fibrous tissue matrix, reduction of oxidative capacity, reduction of  matrix metalloproteinase content, in other words, all the factors that trigger plaque rupture.  

    Though just my suspicion, I believe that the initial relative composition of calcium to plaque of 20% is likely increased, meaning calcium occupies more of total plaque volume. In other words, my suspicion is that, if calcium regresses, total plaque volume has regressed even MORE.

    We plan to publish our data this spring. We had planned to publish our experience much sooner, but the addition of vitamin D to the program has boosted success so much that we decided to start over again around 2 years ago.

  • Anonymous

    12/13/2009 6:34:36 PM |

    hm... bookmarked style Smile)

  • Anonymous

    4/29/2010 4:00:38 AM |

    so great, your arteries are cleared up but you'll get cancer and die from all of those ct scans.
    lovely.

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