Hello everyone and welcome back to the Restorative Health Solutions Blog! We’ve been talking about various testing we recommend in our office and this week’s topic is about cholesterol. If you missed our other articles on thyroid testing, blood testing, stool testing, and hormone testing, please check out some of the links and read those if you have an interest. Let’s move onto cholesterol! As a note this article is not about people who have problems caused by low cholesterol, but rather problems caused by high or seemingly normal cholesterol.

High Cholesterol and Heart Disease: Standard Testing Falls Short

In school we had learned about Cholesterol as a risk marker for heart disease. We learned that HDL cholesterol was “good” and LDL cholesterol was “bad”. Our education also went slightly farther than the television commercials as we learned what VLDL was. Unfortunately that is where our standard medical training basically ended (and probably ended for your doctor too). We did not think about it much until someone brought this statistic to our attention. “50% of patients hospitalized with coronary artery disease had ‘normal’ cholesterol[i]”. If you look up that reference you’ll notice it was published in 2009. Half of the people with heart disease have “normal” cholesterol. What is that about!? We are obviously missing something with the normal cholesterol tests.

As we started doing our own research on cholesterol, heart disease, and other conditions we were surprised that there were other cholesterol markers we had never heard about. Both HDL and LDL had subtypes (like HDL1, HDL2, and HDL3.) Also there was talk about how LDL has these “size patterns” and some people can have different size LDL and these differences can either make the LDL dangerous or benign. We also found something called Lp(a) which seemed to be a significant indicator of heart disease.

[When Dr. Warren spoke with some of his teachers about why students were not learning about these different markers he was told that the current information found in medical research typically takes 15-20 years to work its way into medical training curriculum! Unfortunately this is true in many fields,Thyroid Medication not just heart disease, but that is a topic for another time.]

A standard lipid panel (which you probably got at your last physical) includes:

  1. Total cholesterol
  2. LDL calculated cholesterol
  3. HDL cholesterol
  4. Triglycerides
  5. HDL/Cholesterol ratio.

Most people now are worried if their total cholesterol is over 200. Did you know that the upper range was 260, then 240, then 220, then 200, and now it is considered 180? Rather than focusing on that total cholesterol number, the research really points to testing the types of cholesterol more specifically. Remember the stat we quoted earlier. 50% of patients with heart disease get this test done and it looks normal. Let’s look at a better test and how it can help us.

The Cardiometabolic Panel

The cardiometabolic panel is a much more detailed look at cholesterol than the standard testing.

Here is what the test looks like.

You’ll see how this test still gives the “standard tests” of LDL, HDL, Total Cholesterol, and Triglycerides. However, this test goes deeper. Let’s take a look at just a few markers to see what great information it can provide for us..


HDL is the famous “good cholesterol”. Why is it considered good? HDL generally transports cholesterol from peripheral tissues back to the liver. This means it can take the cholesterol from the plaques in your arteries, clean it up, and return it to the liver. Increased studies are showing that HDL2 is more protective than HDL3[ii],[iii],[iv]. While we are not entirely sure why, it appears HDL2 is more effective in quenching the inflammatory response of atherogenesis[v]. Has anyone tested you for HDL subtypes?

Too make sure we do not hang our hat on only 1 marker lets bring up this point. There was a study published in 1999 that showed HDL2 loses its protective ability in the presence of high triglycerides[vi]. For this reason it is important to realize a high HDL is worthless if you have high triglycerides rendering it ineffective in protecting you against heart disease.

The last point we’ll make on HDL is it can be a bad thing if it is too high. In the presence of inflammation, the nature of the HDL changes and it loses its protective effect[vii]. This is where we get into inflammatory markers like C-reactive protein, NF-kappaB, IL-1beta, IL-6 etc. (An in-depth look at inflammation is our next blog article topic so do not worry if you have not heard of some of these markers!) In our clinic we get worried when we see someone’s HDL above 80. When HDL is above 80 we almost always find major inflammatory issues, which means the protective effect of the HDL is gone.



LDL is commonly known as the “bad” cholesterol. It is responsible mainly for transporting cholesterol from your liver to peripheral tissues. For this reason it brings cholesterol to your arteries and deposits it in your arteries. However, some types of LDL are much worse than others.

If you are worried about high LDL, do you know your density pattern? You can see on this test that LDL1 and LDL2 are large particles and less associated with heart disease than LDL3 and LDL4 which are small. Having small LDL particles (Pattern B) is more dangerous than having large LDL particles (Pattern A). We’ve known since the late 80’s of this pattern. A study published in JAMA in 1988 found this, “The LDL subclass pattern characterized by a preponderance of small, dense LDL particles was significantly associated with a threefold increased risk of myocardial infarction.[viii]”Other studies have also found small LDL particles to be more dangerous than large LDL particles[ix],[x]. Why do people not know about this? It turns out statin drugs are actually most effective at lowering high LDL in the non-threatening Pattern A (large, fluffy LDL particles). If this were more widely stressed statin drugs would be prescribed less…for this reason drug companies have not pushed for more research in this area.


Lp(a) lipoprotein is related to LDL and found to be an important marker for coronary heart disease[xi]. Like LDL its elevation promotes cardiovascular disease. While the exact mechanism for how Lp(a) contributes to heart disease is unknown, we do find it high in populations with cardiovascular disease and lowering it reduces cardiovascular disease[xii]. Why do most people not know about this? There is no drug yet that changes Lp(a), but fortunately for us the cheap, inexpensive, easy to access vitamin B3 (Niacin) has been shown to help lower Lp(a) levels[xiii].

Additional Information

To find out more about the cardiometabolic panel we suggest you go to the Spectracell Labs website or follow the link below:


Another good source of information is Dr. Sinatra who has been interviewed by Dr. Mercola on the VAP test and its benefit in helping to diagnose and aim treatments for cardiovascular diseases.


Other Markers for Heart Disease

Besides the Cardiometabolic panel, there are some other markers that are a must in evaluating heart disease risk.

Inflammation Missing Puzzle PieceHomocysteine

If you are interested in going in depth about homocysteine, please go to our blog post entitled “Homocysteine: A Must Have Test For Anyone With Health Problems“. For now, we’ll just say when there is too much Homocysteine in the blood arteries are damages and plaques form. It is a big deal. In our clinic we want Homocysteine to be below 7. Past 7 we see increased risk for degenerative diseases developing. More information can be found by reading anything from Dr. Kilmer S McCully.

C-Reactive Protein

Cardiovascular disease is not only about cholesterol, but at its root more and more doctors believe it is actually an inflammatory disease. Chronic inflammation in the cardiovascular system leads to degeneration and cholesterol is actually just there to help repair the damage and make sure you don’t “spring a leak”. After all, a bleed in a popped artery will kill you in minutes, but a block from excess plaque build up may take 30 years to kill you. A study published in 2002 entitled Inflammation and Atherosclerosis had this to say, “Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of [atherosclerosis].[xiv]” C-reactive protein is only the beginning of investigating inflammation, but it is a fundamental and absolutely necessary marker to know for your health.

Other Recommended Sources

Other people who have great information if you want to know more about cholesterol and heart disease are Dr. Duane Graveline, Dr. Malcolm Kendrick, Dr. Uffe Ravnskov, and Dr. Kilmer McCully. If you go to Dr. Graveline’s website www.spacedoc.com he actually links these other doctors. For reading we would suggest Dr. Malcolm Kendrick’s The Great Cholesterol Con as the most entertaining cholesterol book of the bunch (some of them are good information but very dry). Dr. Kendrick is rather sarcastic and approaches the problem with a humor that is all together lacking in most books written by doctors J. Make sure you get the book by Malcom Kendrick as there is another author who has a book by the same title.

Another good source of information is Dr. Stephen Sinatra who has been interviewed by Dr. Mercola. You can read a great article from him at the following link.
Read more: http://www.drsinatra.com/cholesterol-levels-optimal#ixzz2GBCzYE3n

That brings us to the end of our talk on cholesterol! As a small recap remember 50% of people with heart disease have “normal cholesterol”. The cardiometabolic panel as well as some other markers like Homocysteine and C-reactive protein are excellent, inexpensive tests that give us much better information.

Another very important factor to keep in mind is inflammation. We briefly touched on it in this article, but inflammation has a role in every chronic disease that currently plagues America. If you are worried about autoimmune diseases, Parkinson’s, Alzheimer’s, Dementia, Heart Disease, Diabetes, Chronic Fatigue, arthritis, or chronic pain, there is an inflammatory component. There are many people who talk about inflammation, but know very little about how it works or different markers of inflammation in the body. Please check out our other blog articles on inflammation for more information.

  • The Restorative Health Solutions Team


[i] Sachdeva A, Cannon CP, Deedwania PC, et al. Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines. Am Heart J. 2009;157(1):111-117.

[ii] Lamarche B, Moorjani S, Cantin B, et al. Associations of HDL2 and HDL3 Subfractions With Ischemic Heart Disease in Men. Arteriosclerosis, thrombosis, and Vascular Biology. 1997; 17:1098-1105.

[iii] Bakogianni M, Kalofoutis A, Skenderi K, Kalofoutis A. Clinical evaluation of plasma high-density lipoprotein subfractions (HDL2, HDL3) in non-insulin-dependent diabetics with coronary arter disease. Journal of diabetes and its complications. 2001; 15:265-269.

[iv] Graham A, Hassal D, Rafique S, Owen J. Evidence for a paraoxonase-independent inhibition of low-density lipoprotein oxidation by high-density lipoprotein. Atherosclerosis. 1997; 135:193-204.

[v] Schafer c, Parlesak A, Eckoldt J, et al. Beyond HDL-cholesterol increase: phospholipid enrichment and shift from HDL3 to HDL2 in alcohol consumers. Journal of Lipid Research. 2007 April; 48:1550-1558.

[vi] Gowri M, Van der Westhuyzen D, Bridges S, Anderson J. Decreased Protection by HDL From Poorly Controlled Type 2 Diabetic Subjects Against LDL Oxidation May Be Due to the Abnormal Composition of HDL. Arteriosclerosis, Thrombosis, and Vascular Biology. 1999; 19:2226-2233.

[vii] Yeap Han C, Chiba T, Campbell J, et atl. Apolipoprotein A-1 and Paraoxonase-1 by Inflammation in Murine Hepatocytes. Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:1806-1813.

[viii] Austin M, Breslow J, Hennekens C, Buring J, et al. Low-Density lipoprotein Subclass Patterns and Risk of Myocardial Infarction. JAMA. 1988;260(13):1917-1921.

[ix] Berneis KK, Krauss RM. Metabolic origins and clinical significance of LDL heterogeneity. J Lipid Res 2002;90:89-94.

[x] Sacks FM, Campos H. Clinical review 163: cardiovascular endocrinology: low-density lipoprotein size and cardiovascular disease: a reparaisal. Clin Endocrinol Metab 2003;884525-32.

[xi] Ghoads G, Dahlen G, Berg K, et al. Lp(a) Lipoprotein as a Risk Factor for Myocardial Infarction. JAMA 1986; 256(18):2540-2544.

[xii] Nordestgaard BG, Chapman M, Ray K, Boren J et al. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J. 2010; Dec;31(23)2844-53.

[xiii] Scanu AM, Bamba R. Niacin and lipoprotein(a): factos, uncertainties, and clinical considerations. American Journal Cardiology. 2008 April:101(8A):44B-7B.

[xiv] Libby P, Ridker P, Maseri A. Inflammation and Atherosclerosis. Circulation. 2002; 105: 1135-1143.

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