CAD AND LDL, HDL AND TRIGLYCERIDE
From Wikipedia, the free encyclopedia
High-density lipoprotein (HDL) is one of the five major groups of lipoproteins, which, in order of sizes, largest to smallest, are chylomicrons, VLDL, IDL, LDL, and HDL, which enable lipids like cholesterol and triglycerides to be transported within the water-based bloodstream. In healthy individuals, about thirty percent of blood cholesterol is
carried by HDL.
Blood tests typically report HDL-C level, i.e. the amount of cholesterol contained in HDL particles. It is often contrasted with low-density
or LDL cholesterol or LDL-C. HDL particles are able to remove cholesterol from within artery atheroma and transport it back to the liver for excretion or re-utilization, which is the main reason why the cholesterol
carried within HDL particles (HDL-C) is sometimes called "good cholesterol" (despite the fact that it is exactly the same
as the cholesterol in LDL particles). Those with higher levels of HDL-C seem to have fewer problems with cardiovascular diseases, while those with low HDL-C cholesterol levels (less than 40 mg/dL or about 1 mmol/L) have increased rates for
heart disease. While higher HDL levels are correlated with cardiovascular health, no incremental increase in HDL has been proven to
improve health. In other words, while high HDL levels might correlate with better cardiovascular health, specifically increasing
one's HDL might not increase cardiovascular health. Additionally, those few individuals producing an abnormal, apparently more efficient, HDL ApoA1 protein variant called ApoA-1 Milano, have low measured HDL-C levels yet very low rates of cardiovascular events even with high blood cholesterol values.
Structure and function
HDL is the smallest of the lipoprotein particles. They are the densest because they contain the highest proportion of protein to cholesterol. Their most abundant apolipoproteins are apo A-I and apo A-II. The liver synthesizes these lipoproteins as complexes of apolipoproteins and phospholipid, which resemble cholesterol-free
flattened spherical lipoprotein particles. They are capable of picking up cholesterol, carried internally, from cells by interaction
with the ATP-binding cassette transporter A1 (ABCA1). A plasma enzyme called lecithin-cholesterol acyltransferase (LCAT) converts the free cholesterol into cholesteryl ester (a more hydrophobic form of cholesterol), which is then sequestered
into the core of the lipoprotein particle, eventually making the newly synthesized HDL spherical. They increase in size as
they circulate through the bloodstream and incorporate more cholesterol and phospholipid molecules from cells and other lipoproteins,
for example by the interaction with the ABCG1 transporter and the phospholipid transport protein (PLTP).
HDL transports cholesterol mostly to the liver or steroidogenic organs such as adrenals, ovary, and testes by direct and indirect pathways. HDL is removed by HDL receptors such as scavenger receptor BI (SR-BI), which mediate the selective uptake of cholesterol from HDL. In humans, probably the most relevant pathway is the
indirect one, which is mediated by cholesteryl ester transfer protein (CETP). This protein exchanges triglycerides of VLDL against cholesteryl esters of HDL. As the result, VLDLs are processed to LDL, which are removed from the circulation by the LDL receptor pathway. The triglycerides are not stable in HDL, but degraded by hepatic lipase so that finally small HDL particles are left, which restart the uptake of cholesterol from cells.
The cholesterol delivered to the liver is excreted into the bile and, hence, intestine either directly or indirectly after conversion into bile acids. Delivery of HDL cholesterol to adrenals, ovaries, and testes is important for the synthesis of steroid hormones.
Several steps in the metabolism of HDL can contribute to the transport of cholesterol from lipid-laden macrophages of atherosclerotic arteries, termed foam cells, to the liver for secretion into the bile. This pathway has been termed reverse cholesterol transport and is considered as the classical protective function of HDL toward atherosclerosis.
However, HDL carries many lipid and protein species, several of which have very low concentrations but are biologically
very active. For example, HDL and their protein and lipid constituents help to inhibit oxidation, inflammation, activation of the endothelium, coagulation, and platelet aggregation. All these properties may contribute to the ability of HDL to protect from atherosclerosis, and it is not yet known what
are the most important.
In the stress response, serum amyloid A, which is one of the acute-phase proteins and an apolipoprotein, is under the stimulation of cytokines (IL-1, IL-6), and cortisol produced in the adrenal cortex and carried to the damaged tissue incorporated into HDL particles. At the inflammation site, it attracts and activates leukocytes.
In chronic inflammations, its deposition in the tissues manifests itself as amyloidosis.
It has been postulated that the concentration of large HDL particles more accurately reflects protective action, as opposed
to the concentration of total HDL particles. This ratio of large HDL to total HDL particles varies widely and is measured only by more sophisticated lipoprotein
assays using either electrophoresis (the original method developed in the 1970s) or newer NMR spectroscopy methods (See also: NMR and spectroscopy), developed in the 1990s.
Men tend to have noticeably lower HDL levels, with smaller size and lower cholesterol content, than women. Men also have
an increased incidence of atherosclerotic heart disease. Alcohol consumption tends to raise HDL levels, and moderate alcohol consumption is associated with lower cardiovascular and all-cause mortality.
Epidemiological studies have shown that high concentrations of HDL (over 60 mg/dL) have protective value against cardiovascular diseases such as ischemic stroke and myocardial infarction. Low concentrations of HDL (below 40 mg/dL for men, below 50 mg/dL for women) increase the risk for atherosclerotic diseases.
Data from the landmark Framingham Heart Study showed that, for a given level of LDL, the risk of heart disease increases 10-fold as the HDL varies from high to low. On
the converse, however, for a fixed level of HDL, the risk increases 3-fold as LDL varies from low to high.
Even people with very low LDL levels are exposed to increased risk if their HDL levels are not high enough.
Estimating HDL via associated cholesterol
Many laboratories used a two-step method: Chemical precipitation of lipoproteins containing apoprotein B, then calculating
HDL associated cholesterol as the cholesterol remaining in the supernate, and there are also direct methods. Both methods have long been promoted on the basis of lowest cost, though neither
of these measurements directly, or reliably, reflects HDL particle functionality to remove cholesterol from atherosclerotic
plaque and can therefore be misleading, especially on an individual patient-by-patient basis Labs use the routine dextran sulfate-Mg2+ precipitation method with ultracentrifugation/dextran sulfate-Mg2+
precipitation as reference method. HPLC can be used.
Subfractions (HDL-2C, HDL-3C) can be measured and have clinical significance.
The American Heart Association, NIH and NCEP provides a set of guidelines for fasting HDL levels and risk for heart disease.
|<40 for men, <50 for women
||Low HDL cholesterol, heightened risk for heart disease|
||Medium HDL level|
||High HDL level, optimal condition considered protective against heart disease|
Low LDL with low HDL level is also risk factor for cardiovascular disease.
Measuring HDL concentration and sizes
As technology has reduced costs and clinical trial have continued to demonstrate the importance of HDL, methods for directly
measuring HDL concentrations, and size (which indicates function) at lower costs have become increasingly available and regarded
as more important for assessing individual risk for progressive arterial disease and improve treatment methods.
HDL, as discussed above, forms from two large proteins, predominantly apo A-I and apo A-II, positioned, back to back. Charged amino acids on the outer surface attract water, making the particles both water-soluble
(so as to carry fats within the blood) and able to associate with HDL receptors on in the surface of cells, e.g. the macrophages of which plaque is predominantly composed, at least in the early stages. Cholesterol is carried within and between the two particles. If
the particles pick up more cholesterol, then the particles enlarge and a third or fourth apo A protein joins the grouping,
termed large HDL. Chemical measurements can be used to estimate HDL concentrations present in a blood sample, though such
measurements may not indicate how well the HDL particles are functioning to reverse transport cholesterol from tissues. HDL-cholesterol
is measured by first removing LDL particles by aggregation or precipitation with divalent ions (such as Mg++) and then coupling
the products of a cholesterol oxidase reaction to an indicator reaction. The measurement of apo-A reactive capacity can be
used to measure HDL cholesterol but is thought to be less accurate.
Since the HDL particles have a net negative charge and vary by size, electrophoresis measurements have been utilized since the 1960s to both indicate the number of HDL particles and additionally sort them by
size. Larger HDL particles are carrying more cholesterol.
The newest methodology for measuring HDL particles, available clinically since the late 1990s 
Nuclear Magnetic Resonance
fingerprinting of the particles to measure both concentration and sizes. This methodology has reduced costs relative to ultracentrifugation.
Optimal Total and Large HDL concentrations
The HDL particle concentrations are typically categorized by event rate percentiles based on the people participating and
being tracked in the MESA 
a medical research study sponsored by the United States National Heart, Lung, and Blood Institute.
Total HDL particle Table
||Total HDL particles μmol/L
||Those with highest (Optimal) total HDL particle concentrations & lowest rates of cardiovascular disease events|
||Those with moderately high total HDL particle concentrations & moderate rates of cardiovascular disease events|
||Those with lower total HDL particle concentrations & Borderline-High rates of cardiovascular disease|
||Those with lowest total HDL particle concentrations & Highest rates of cardiovascular disease events|
Large (protective) HDL particle Table
||Large HDL particles μmol/L
||Those with highest (Optimal) Large HDL particle concentrations & lowest rates of cardiovascular disease events|
||Those with moderately high Large HDL particle concentrations & moderate rates of cardiovascular disease events|
||Those with lower Large HDL particle concentrations & Borderline-High rates of cardiovascular disease|
||Those with lowest Large HDL particle concentrations & Highest rates of cardiovascular disease events|
low LDL level with The lowest incidence of atherosclerotic events over time occurs within those with both the highest concentrations
of total HDL particles, the top quarter (>75%), and the highest concentrations of large HDL particle concentrations. Multiple
other measures, including LDL particle concentrations, small LDL particle concentrations, along with VLDL concentrations,
estimations of Insulin resistance pattern and standard cholesterol lipid measurements (for comparison of the plasma data with the estimation methods discussed
above) are also routinely provided.
Fasting serum lipids have been associated with short term verbal memory. In a large sample of middle aged adults, low HDL
cholesterol was associated with poor memory and decreasing levels over a five year follow-up period were associated with decline
Increasing HDL levels
Diet and lifestyle
Certain changes in lifestyle may have a positive impact on raising HDL levels:
Most saturated fats increase HDL cholesterol to varying degrees but also raise total and LDL cholesterol. A high-fat, adequate-protein, low-carbohydrate ketogenic diet may have similar response to taking niacin as described below (lowered LDL and increased HDL) through beta-hydroxybutyrate coupling the Niacin receptor 1.
While higher HDL levels are correlated with cardiovascular health, no increase in HDL has been proven to improve health.
In other words, while high HDL levels might correlate with better cardiovascular health, specifically increasing one's HDL
might not increase cardiovascular health. Pharmacological therapy to increase the level of HDL cholesterol includes use of fibrates and niacin. Fibrates have not been proven to have an effect on overall deaths from all causes, despite their effects on lipids. Similarly, increased HDL levels from niacin have not been shown to be efficacious in reducing cardiovascular disease
in a randomized controlled trial.
Niacin (vitamin B3), increases HDL by selectively inhibiting hepatic Diacylglycerol acyltransferase 2, reducing triglyceride synthesis and VLDL secretion through a receptor HM74 otherwise known as Niacin receptor 2 and HM74A / GPR109A, Niacin receptor 1.
Pharmacologic (1- to 3-gram/day) niacin doses increase HDL levels by 10–30%, making it the most powerful agent to increase HDL-cholesterol. A randomized clinical trial demonstrated that treatment with niacin can significantly reduce atherosclerosis progression
and cardiovascular events. However, niacin products sold as "no-flush", i.e. not having side-effects such as "niacin flush", do not contain free nicotinic acid and are therefore ineffective at raising HDL, while products sold as "sustained-release"
may contain free nicotinic acid, but "some brands are hepatotoxic"; therefore the recommended form of niacin for raising HDL
is the cheapest, immediate-release preparation. Both fibrates and niacin increase artery toxic homocysteine, an effect that can be counteracted by also consuming a multivitamin with relatively high amounts of the B-vitamins, however multiple European trials of the most popular B-vitamin cocktails, trial showing 30% average reduction
in homocysteine, while not showing problems have also not shown any benefit in reducing cardiovascular event rates. A 2011
niacin study was halted early because patients showed no increase in heart health, but did experience an increase in the risk
In contrast, while the use of statins is effective against high levels of LDL cholesterol, it has little or no effect in raising HDL cholesterol.
Lovaza has been shown to increase HDL-C.
Magnesium supplements raise HDL-C.
Apo-A1 Milano, the most effective proven HDL agent, is in commercial production by a Canadian company, Sembiosys, but as of 2010 may still
be several years away from clinical availability.
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. Journal of epidemiology and community health 40 (3): 249–256. PMC 1052533
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"National Institutes of Health", 2003 Jan–Feb. Accessed 2011 May 31.
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. The Cleveland Clinic Heart and Vascular Institute. Retrieved
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M.; Katan, Martijn B. (2003). "Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on
serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials"
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acid receptor subtypes and their ligands". Medicinal Research Reviews 27 (3): 417–33. doi:10.1002/med.20102
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The New Zealand medical journal 120 (1261): U2706. PMID 17853928
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therapy in atherosclerosis". Current opinion in lipidology 15 (6): 659–65. doi:10.1097/00041433-200412000-00006
- ^ Rader, Daniel J. (2004). "Raising HDL in Clinical Practice"
Raising HDL in Clinical Practice: Clinical Strategies to Elevate HDL. Retrieved 8
- ^ a b Brewer, H. Bryan (27 December 2005). "Raising HDL-Cholesterol and Reducing Cardiovascular Risk: An Expert Interview With H. Bryan Brewer, Jr,
. Retrieved 8 October 2009.
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Shepherd, James; Sirtori, Cesare; European Consensus Panel on HDL-C (2004). "Raising high-density lipoprotein cholesterol
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Panel on HDL-C". Current medical research and opinion 20 (8): 1253–68. doi:10.1185/030079904125004402
- ^ Drexel, H. (2006). "Reducing risk by raising HDL-cholesterol:
the evidence". European Heart Journal Supplements 8: F23. doi:10.1093/eurheartj/sul037
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John D. (2003). "Varying Cost and Free Nicotinic Acid Content in Over-the-Counter Niacin Preparations for Dyslipidemia"
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- ^ http://www.npr.org/blogs/health/2011/05/28/136678665/study-boosting-good-cholesterol-with-niacin-did-not-cut-heart-risks?ps=sh_sthdl
- ^ http://us.gsk.com/products/assets/us_lovaza.pdf
- ^ Rosanoff A, Seelig MS (October 2004). "Comparison of mechanism and functional effects of magnesium and statin pharmaceuticals"
J Am Coll Nutr 23 (5): 501S–505S. PMID 15466951
"HMG CoA Reductase is an important enzyme in lipid and cholesterol metabolism, but it is not the only one. The statins act
by inhibiting, temporarily, the enzyme, in a dose response relationship whereas the magnesium ion (Mg2+) is an important part
of a complex control and regulation of this important pathway. Both lower LDL-C, some statins can raise HDL-C and lower triglycerides,
but Mg supplements do both quite reliably."
HAD : TRIGLYCERIDE = 1:<2 is optimal
HDL has two kinds of particles: Small and large and floppy
Believe it or not I have somewhat elevated blood cholesterol numbers and I just received the latest data from my doctor.
But being the typical numbers geek, I want to analyze the numbers to death just for the sheer joy of it. First, off there
does not seem to be a good working "find the missing value" calculator for cholesterol numbers on the internet when the math
is so incredibly easy. Enter any three
of the following numbers and the calculator will find the fourth
missing value, and then it will tell you the ratios and how good they are. You can read the article from the American Heart
Association on desired levels here.
. The articles on the Total Cholesterol/HDL and HDL/LDL ratios from eMedTV can be found here
, and the article on triglycerides over HDL ratio is here.
- Accurate - The accuracy of VAP measurements
are verified by beta quantification, a standard procedure for lipoprotein
- Affordable - The VAP Test is reimbursed by
most insurance carriers and Medicare/Medicaid.
You can find out
by contacting Atherotech.
- Accessible - Obtaining a VAP Test is easy.
Contact your local clinical lab, or obtain a VAP
by contacting Atherotech.
Download Accuracy Data (pdf)
- Easy – Because we are directly measuring LDL-C, fasting is not required.
- Effective – By reporting 22 different components of cholesterol, the VAP Test identifies
risks you can't
see with a standard lipid panel.
More Comprehensive Test
The VAP Test uses an advanced technology
that provides a more accurate, individualized picture of your heart disease and diabetes risk so you and your doctor can take
steps to prevent a future heart attack. For example, the VAP Expanded Lipid Profile measures not only the basic information
provided by the routine cholesterol test, but also identifies hidden cholesterol problems that can increase your risk of developing
heart disease or diabetes—even if your routine cholesterol test results are "normal." As a result, the VAP Test was
named one of "Ten Ways to Live Longer" by Forbes.com and was selected as one of "Five Tests Worth Paying For" by The Wall
Why the Need for a VAP Test
Heart disease is the leading killer
of both men and women in the United States—causing the deaths of more than 500,000 people each year. Unfortunately,
getting "normal" results back from a routine cholesterol test doesn't mean one is safe from heart disease. That's because
routine cholesterol tests fail to identify half of those at risk—robbing many people of the opportunity to take preventive
steps that might save their lives.
The VAP Test provides valuable information that can identify hidden heart disease risks. It breaks
down cholesterol beyond HDL (high-density lipoprotein, the "good" cholesterol), LDL (low-density lipoprotein, the "bad" cholesterol),
and triglycerides—providing new information that can help your doctor better assess and manage your heart disease risk.
VAP Tests also help identify the metabolic syndrome-which leads to diabetes and heart disease, and affects a staggering 55
The role of cholesterol testing in clinical
practice is to stratify a patient's risk for cardiovascular disease and to direct therapy to reduce that risk. Accuracy and
comprehensiveness in cholesterol testing are critical, especially in light of lower LDL goals, as well as the need to measure
and treat a variety of cholesterol subclasses and components. As a result, the heart disease and diabetes risk factors reported
by the the VAP Test technology are the best choice for patients at risk for cardiometabolic disorders.
Apolipoprotein B100 (apoB100)
Several studies have shown that
apolipoprotein B (apoB) is a better risk predictor for coronary heart disease (CHD) than several other risk factors, including
LDL cholesterol., Since each atherogenic lipoprotein (Lp(a), LDL, IDL, and VLDL) contains one molecule of apoB, apoB
concentration therefore represents the total number of atherogenic particles. Atherotech has developed a novel procedure to
report apoB utilizing non-HDL-cholesterol along with lipoprotein density distribution using the patented VAP ultracentrifugation
method. Atherotech has thoroughly validated this new procedure by comparing the VAP apoB with measured apoB using serum from
1,797 patients. This comparison has yielded an excellent correlation coefficient (r = 0.97) with bias of only 0.8%.
1. AMORIS Study, Lancet, 2001; 358: 2026-33.
2. Health Professionals Follow-Up Study, Circulation, 2005; 112: 3375-83.
One of the key benefits of the VAP technology
is a direct-measured LDL. The routine cholesterol panel, which estimates LDL using the Friedewald formula, provides only a
40% predictive value for coronary heart disease. In contrast, the VAP Test, which directly measures LDL, identifies a far
greater number of patients at risk for heart disease.
Because of the concerns regarding the reliability of estimated LDL, the NCEP ATP III guidelines recommend
that direct LDL measurement methods be used as they are unaffected by triglycerides and patient fasting. In fact, estimated
LDL cholesterol levels become significantly inaccurate in patients with heart disease or the equivalent (LDL goal <70-100
mg/dL). Estimated LDL cholesterol levels often fail to accurately classify risk for those patients with triglycerides >200
How to get a VAP Test
Obtaining a VAP Test is easy. Your physician
refer you to a local clinical lab to handle the test,
which requires just a small blood sample. The
is reimbursed by most insurance carriers
and Medicare/Medicaid. You can also obtain a VAP
Test directly by contacting Atherotech.
View a sample (pdf)
NCEP ATP III Secondary Targets of Therapy and Emerging Risk Factors
addition to the LDL cholesterol level, the VAP technology also reports the NCEP ATP III secondary targets of therapy and emerging
risk factors, which play a role in raising a patient's level of risk. Measuring these risk factors is the key to managing
atherogenic dyslipidemia, setting more aggressive LDL goals, and providing expanded indications for therapy.
- Increased remnant lipids (intermediate-density lipoprotein and small very low-density lipoprotein) are candidates for
intervention, and can heighten heart disease risk substantially beyond that predicted by LDL alone.
- The presence of the "lipid triad" (small LDL, low HDL and elevated triglycerides) of the metabolic syndrome is considered,
as a whole, a risk factor.
- LDL Pattern B is an indication of atherogenic dyslipidemia and the metabolic syndrome.
- Elevated levels of lipoprotein(a) are an independent risk factor for heart disease.
Patients with abnormal screening profiles or positive family history also benefit from identification
of secondary and emerging risk factors. These may be used along with clinical judgment to raise a patient's risk classification,
lower their target LDL goal, and/or modify their treatment plan.
Atherotech offers a comprehensive education program
designed to increase physician understanding and use of advanced lipid testing in clinical practice. Included are presentations,
articles, and other educational materials. Contact Atherotech for more information.
The VAP (vertical auto profile) test is a cholesterol, lipid and lipoprotein test. The name "VAP test" was coined by the privately held cardio-diagnostic company Atherotech to identify their direct-measurement method which categorizes not just total cholesterol, high-density lipoproteins (HDL), and low-density lipoproteins (LDL), but all lipids and subclasses, with an LDL measurement accuracy unaffected by triglycerides.
Atherotech claims their VAP test has a unique ability to identify far more areas of risk to patients than the standard
lipid panel, specifically because it reports 15 separate components versus four in the standard cholesterol test. The more
comprehensive test was shown to identify more than twice the number of patients with lipid abnormalities than the standard lipid panel (cholesterol
and triglyceride test).
Unlike the standard lipid panel, the VAP test directly measures LDL. The test is also the only commercially available test
that meets the new American Diabetes Association and American College of Cardiology (ADA-ACC) cholesterol guidelines for people
at high risk of heart attack and stroke (including people with Type 2 diabetes). The ADA-ACC consensus statement establishes
measurement and treatment guidelines for apoB in addition to LDL and non-HDL in high-risk patients. The VAP test is the first cholesterol profile to comply with updated
National Cholesterol Education Program ATP III recommendations for LDL measurement and the only commercially available advanced
lipid profile that routinely reports all three lipoprotein parameters considered necessary by the American Diabetes Association and American College of Cardiology expert consensus guidelines.
People with a family history or an existing condition of diabetes, high blood pressure or heart disease—or who are
already taking cholesterol lowering medication—are candidates for the comprehensive VAP (vertical auto profile) test.
In addition, those who don't score within the desirable ranges of the standard cholesterol test can opt for the more detailed
test to assist in improved diagnosis by their physician.
- ^ http://www.thevaptest.com
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For Francis Crick and James Watson, it was discovering DNA.
even these men of great infamy were not given the immediate critical acclaim and accolades from their peers that such displays
of cerebral excellence deserved in their own time. It wasn't until years later in the context of historical significance that
each of these discoveries and works of art became known as the brilliant showpieces they are today.
Now we have another
candidate that fulfills the litmus test for genius and yet his work is not being heralded by the people of his generation
as it deserves to be. I suppose he should feel proud to be placed in the same company as an Einstein, da Vinci, or Crick and
Watson because his discoveries about cholesterol are no less spectacular than what they found.
Remember the name: Anthony
Colpo. His book is called The Great Cholesterol Con
. If ever there was a more compelling health book in my lifetime that has the potential to directly influence the decisions
of so many doctors, patients, and researchers on the subject of cholesterol, then I haven't seen it. And yet, how many people
have even heard of Colpo and his prodigious independent research?
Not many...yet! But I expect that to change rather
quickly as word about this 368-page dissertation about the biggest health scam of the 21st Century spreads from those of us
who have had the privilege of experiencing this great work by Colpo.
It literally took me weeks to get through and
absorb all of the information contained within the pages of this amazing book, but it was defintely NOT a boring, laborious
book of scientific annotations that will go completely over your heard. Colpo writes in a meticulous style that leaves no
stone unturned while also captivating your attention with head-on language he dares you to ignore. The time and energy it
must have taken him to write his very first and probably best book of his career is clearly evident in page turn after every
glorious page turn.
Colpo is a brave fighter who is unafraid to expose the medical and research community for perpetrating
an outright fraud on a public who is either too ignorant or uneducated to question their conclusions regarding health. That's
why statin drugs have become one of the top moneymakers for drug companies today because of this false illusion that everyone
"needs" to artificially lower their cholesterol for the sake of their heart health. LIAR!
The big secret that Colpo
exposes is the FACT that the rate of heart disease has not decreased one iota since the introduction of statins, such as Lipitor
and Crestor, and yet you never hear anybody ever talking about this. Why?
Furthermore, the suspicious side effects
of taking these expensive medications, including intense joint and muscle pain, are swept under the rug as a necessary part
of treating cholesterol. What a big fat joke this "great cholesterol con" has become!
As someone who has been fooled
into taking these drugs all "for the sake of my health," it angered me that I could be so duped by the very doctors that I
trust to provide me with the best medical care possible. Thankfully for me I was able to come off of the cholesterol-lowering
drugs after losing 180 pounds on the low-carb lifestyle. But not everyone is able to figure this out on their own, which is
why Colpo's book has been so sorely needed for far too long.
Colpo really does deserve a medal for putting himself
out there as the direct target of the drug manufacturers, pharmaceutical reps, and doctors who have been making BILLIONS of
dollars in profit off of this scheme for far too long. If you aren't outraged about this as much as Colpo is, then you REALLY
need to read his book as soon as possible. It will open your eyes to an underground world of corruption and deceit that is
jeopardizing the very health of the world's population.
Does this sound like a conspiracy of some sort? I suppose it
has those markings. But Colpo is DEAD serious and provides all the references you need to see for yourself how this "great
cholesterol con" has been allowed to exist. This book should be a warning to everyone who thinks taking that cholesterol-lowering
drug will protect them against a heart attack or heart disease. It's time to stop letting others think for you and to start
thinking for yourself by arming yourself with the facts.
In addition to cholesterol, Colpo also gets into such issues
as how saturated fat and low-carb diets have been unfairly maligned as health threats while behind-the-scenes they are being
proven by new scientific evidence to be a lot healthier and safe for weight and health management than the failed low-fat
diets ever will be. My weight loss experience is living proof of that!
An eyeopener for sure, The Great Cholesterol Con
will one day become required reading for medical students wanting to find out the truth about cholesterol, diet and
heart disease. It is Colpo's genius that we should be celebrating for coming along at this point in time in the history of
the world to be the beacon of truth for all the world to see.
Will you remain blinded by the lies you've been told
or will you become enlightened by the invaluable information Colpo has provided as his gift to the world? That's a decision
YOU and you alone must make which can impact your life more than you even realize regardless of what you choose to do.
if you decide to have your eyes opened, do you keep it to yourself or will you also share it with your friends and family?
This is the kind of book that every living man, woman, and child should have to read just once.
If you decide to reject
what is contained within the book, then at least you'll be armed with the facts.
But if instead you decide to embrace
what you've read and be moved to action, then the legend of Colpo will rise beyond this mundane world of ours to metamorphose
into a greater understanding of what healthy living is really all about.
When that happens, the genius of Colpo will
FINALLY be recognized and he will take his rightful place in history behind those great names of the past for what he has
contributed to the world.
Remember the name: Anthony Colpo.
Labels: Anthony Colpo, book, cholesterol, Great Cholesterol Con, review
Clinics. 2008 August; 63(4): 427–432.
High Ratio of Triglycerides to HDL-Cholesterol Predicts Extensive Coronary Disease
This article has been cited by
other articles in PMC.
An abnormal ratio of triglycerides to HDL-cholesterol (TG/HDL-c) indicates an atherogenic lipid profile and a risk
for the development of coronary disease.
To investigate the association between lipid levels, specifically TG/HDL-c, and the extent of coronary disease.
High-risk patients (n = 374) submitted for coronary angiography had their lipid variables measured and coronary
disease extent scored by the Friesinger index.
The subjects consisted of 220 males and 154 females, age 57.2 ± 11.1 years, with total cholesterol of 210± 50.3
mg/dL, triglycerides of 173.8 ± 169.8 mg/dL, HDL-cholesterol (HDL-c) of 40.1 ± 12.8 mg/dL, LDL-cholesterol (LDL-c) of 137.3
± 46.2 mg/dL, TG/HDL-c of 5.1 ± 5.3, and a Friesinger index of 6.6 ± 4.7. The relationship between the extent of coronary
disease (dichotomized by a Friesenger index of 5 and lipid levels (normal vs. abnormal) was statistically significant for
the following: triglycerides, odds ratio of 2.02 (1.31–3.1; p = 0.0018); HDL-c, odds ratio of 2.21 (1.42–3.43;
p = 0.0005); and TG/HDL-c, odds ratio of 2.01(1.30–3.09; p = 0.0018). However, the relationship was not significant
between extent of coronary disease and total cholesterol [1.25 (0.82–1.91; p = 0.33)] or LDL-c [1.47 (0.96–2.25;
p = 0.0842)]. The chi-square for linear trends for Friesinger > 4 and lipid quartiles was statistically significant for
triglycerides (p = 0.0017), HDL-c (p = 0.0001), and TG/HDL-c (p = 0.0018), but not for total cholesterol (p = 0.393) or LDL-c
(p = 0.0568). The multivariate analysis by logistic regression OR gave 1.3 ± 0.79 (p = .0001) for TG/HDL-c, 0.779 ± 0.074
(p = .0001) for HDL-c, and 1.234 ± 0.097 (p = 0.03) for LDL. Analysis of receiver operating characteristic curves showed that
only TG/HDL-c and HDL-c were useful for detecting extensive coronary disease, with the former more strongly associated with
Although some lipid variables were associated with the extent of coronary disease, the ratio of triglycerides to
HDL-cholesterol showed the strongest association with extent.
Keywords: Lipids, Triglycerides, HDL, Cholesterol, Coronary
Lipid abnormalities have long been suspected to contribute to atherosclerosis; several epidemiological and cohort
studies have established a strong association between total cholesterol, LDL-cholesterol (LDL-c), or low HDL-cholesterol (HDL-c)
and the incidence of atherosclerosis-related diseases, such as ischemic heart disease, stroke, and peripheral vascular disease.
Recently, lipid particle subfractions have also been implicated in the atherogenic process. Small dense LDL particles
are more atherogenic than larger buoyant ones, and different HDL subfractions play different roles in atherogenesis. The larger
and less dense HDL2 particles are considered protective, while the small dense HDL3 particles are atherogenic.1,2 The former correlate inversely with serum triglycerides and small dense LDL.3 The ratio of triglycerides to HDL-cholesterol ratio (TG/HDL-c) correlates inversely with the plasma level of small,
dense LDL particles. A TG/HDL-c ratio of 3.8 divides the distribution of LDL phenotypes, with 79% of phenotype B greater than
this value, and 81% of phenotype A lower than this value4. We recently analyzed the relationship between plasma lipids and development of coronary artery disease (CAD) as manifested
by angina, positive ischemic tests, or significant obstructive lesions in the coronary angiogram. We found that an TG/HDL-c
ratio >4 is the most powerful independent predictor of CAD development5. Thus, this ratio shows promise as an attractive surrogate index of the atherogenicity of the plasma lipid profile.
However, little data exist on the association between TG/HDL-c ratio and the extent or severity of lesions in coronary disease.
To evaluate the correlation between lipid variables, especially the TG/HDL-c ratio, and the extent of coronary
disease in patients investigated for suspected CAD.
Eligible patients were outpatients who underwent diagnostic coronary angiography for suspected coronary disease.
The presence of risk factors were defined as follows: hypercholesterolemia (total cholesterol >200 mg/dL),
hypertriglyceridemia (>150 mg/dL), high LDL-cholesterolemia (LDL-c) (>130 mg/dL), low HDL-cholesterolemia (HDL-c) (<40
mg/dL for male and <50 mg/dL for female), elevated TG/HDL-c ratio (>4), diabetes mellitus (fasting glucose ≥ 126
mg/dL, casual or GTT over 200 mg/dL, or current use of oral hypoglycemiant or insulin), hypertension (cutoff points were 140/90
mm Hg), and status as a current smoker.
Laboratory tests for total cholesterol and fractions, triglycerides, and glycemia were performed using standard
Coronary lesion extent was evaluated using the Friesinger index6. This classification uses the following categories: 0, no arteriographic abnormalities; 1, trivial irregularities (lesions
from 1–29%); 2, lesions from 30–68%; 3, multiple narrowing in the same vessel, and the segment has either one
lesion with a morphology defined as multiple, diffuse or tubular, or two segments with stenosis of 30–68%; 4, at least
one lesion of 69–100%, except in the proximal segment where it should be less than 100%; and 5, occlusion of a proximal
segment of a vessel. Left main lesions were counted as proximal lesions of both left descending and circumflex arteries. Coronary
lesions were scored by experts blinded to patient lipid profiles.
Statistics were calculated by univariate analysis with chi-square and non-parametric ANOVA (Kruskal-Wallis), followed
by multivariate analysis using stepwise forward logistic regression to assess the independent influence of lipid variables
on extent of coronary disease extension, dichotomized by a Friesinger index of 5.
The subjects included 374 patients, 165 (60.2%) men and 109 (39.8%) women, with a mean age of 57 ± 11.5 years.
Total cholesterol was 214 ± 50.2 mg/dL; triglycerides, 167.9±91.7 mg/dL; HDL-c, 38.5 ± 11.9 mg/dL; LDL-c, 142.9 ± 45 mg/dL;
TG/HDL-c, 5.1 ± 4.0; and Friesinger index, 6.9 ± 4.4. Hypertensive and dyslipidemic subjects were predominantly male. shows demographics of the patient sample, as well as the distribution of coronary lesions.
Demographic characteristics of patient sample and Friesinger index frequency
Extensive coronary disease, by univariate analysis, presented a direct relationship with the quartiles of total
triglycerides, and TG/HDL-c, and an inverse relationship with HDL-c quartiles ().
Frequency of extensive coronary disease (Friesinger index ≥5) by lipid quartile
The odds ratios for the extent of coronary disease between the fourth and first quartiles were as follows: total
cholesterol, 1.08, 95%CI (0.57–2.03), p = 0.87; LDL-c, 1.62, 95%CI (0.86–3.06), p = 0.15; triglycerides, 1.7,
95%CI (0.94–3.08), p = 0.986; HDL-c, 0.25, 95%CI (0.13–0.46), p = 0.0001; and TG/HDL-c, 3.31, 95%CI (1.78–6.14),
p = 0.0002 (). This analysis showed that only HDL-c and TG/HDL-c show statistically significant frequency differences between the fourth
and first quartiles, and that the difference was larger for TG/HDL-c. The non-parametric ANOVA (Kruskal-Wallis) demonstrated
a significant association between extensive coronary disease and the lipid variable quartiles. However, only HDL-c and TG/HDL-c--primarily
the latter--showed statistically significant differences in median Friesinger index between abnormal values and normal ones.
Total cholesterol and LDL-c showed a similar distribution and therefore presents only the Friesinger distribution for the quartiles of total cholesterol, triglycerides, HDL-c, and TG/HDL-c.
Odds ratios between fourth and first quartiles of lipid variables for extensive coronary disease (Friesinger index
Boxplot distribution of Friesinger index by quartiles of total cholesterol, triglycerides, HDL-cholesterol, and
The multivariate analysis by logistic regression included these lipid variables, and it showed that the TG/HDL-c
ratio showed the strongest correlation [association] with extent of coronary disease. Increasing the HDL-c quartile led to
a 22% decrease in extent, while increasing the LDL-c or TG/HDL-c quartiles led to a 23% and 30% increase in disease extent,
Results of multivariate analysis
Of the 246 subjects with low HDL-c, 171 (69.5%) had extensive coronary disease, and of the 170 subjects with high
TG/HDL-c, 122 (72%) had extensive coronary disease. This may be due to the fact that HDL-c and Triglycerides levels were discordant
in 35 (25%) of subjects with low extents of disease and in 75 (32%) of subjects with extensive coronary disease. Thus, taking
both variables into account by using the Triglycerides to HDL-c ratio increased the accuracy of detecting extensive coronary
Analysis of the ROC curves showed the following areas under the curves: 0.35 for HDL-c (p = 0.0001), 0.55 for
LDL-c (p = 0.131), and 0.63 for TG/HDL-c (p = 0.0001).
We found a relationship between the extent of coronary disease and lipid variables using univariate analysis.
In a multivariate model that included these variables, the ratio of triglycerides to HDL-cholesterol was found to be a powerful
independent indicator of extensive coronary disease.
Despite the fact that small, dense LDL particles are an established risk factor for cardiovascular disease, the
assessment of their subfractions by current methods have been too technically demanding to be applicable in a routine clinical
laboratory. The usual techniques include density gradient ultracentrifugation,7 non-denaturing gradient gel electrophoresis (NDGGE),8 and nuclear magnetic resonance (NMR) spectroscopy,9 which have the disadvantages of being labor-intensive, technically demanding, expensive, or slow to produce results.
As a result, these precise and accurate techniques are not widely used in clinical settings. Thus, developing surrogate markers
of lipid particle profiles are of great clinical and economic importance.
Several studies have attempted to determine the risk levels for CAD using lipid indexes or formulas.10 The goal of this work is to manage patients better in order to prevent cardiac events. Of particular interest are ratios
that have atherogenic particles in the numerator and HDL-c or its constituents in the denominator. The ratio of total cholesterol
to HDL-c11,12 and, to a lesser extent, the ratio of LDL-c to HDL-c13 have been shown to be better predictors of CAD than lipid alone. More recently, in the INTERHEART case-control study,
the apoB/apoA1 ratio was shown to be the strongest risk factor associated with myocardial infarction.14 This ratio had already been proposed as an accurate predictor of risk for major coronary events in the AFCAPS/TexCAPS15 and AMORIS16 studies.
The ratio TG/HDL-c, initially proposed by Gaziano et al,17 is an atherogenic index that has proven to be a highly significant independent predictor of myocardial infarction,
even stronger than TC/HDL-c and LDL-c/HDL-c. The Copenhagen Male Study showed triglycerides on their own to be another strong
risk factor, but it found that stratifying triglyceride levels by HDL-c levels led to more accurate detection of increased
risk of coronary disease.18
The atherogenic link between high triglycerides and HDL-c is due to the higher plasma concentration of triglyceride-rich,
very low-density lipoprotein that generates small, dense LDL during lipid exchange and lipolysis. These LDL particles accumulate
in the circulation and form small, dense HDL particles, which undergo accelerated catabolism, thus closing the atherogenic
The present study indicates that TG/HDL-c, which we previously showed to be an indicator of development of coronary
heart disease development,5 is also related to the severity of vessel compromise. Thus this ratio is an easy, non-invasive means of predicting
the presence and extent of coronary atherosclerosis.
We studied a high-risk subset of patients, who showed a higher prevalence of coronary disease than the general
population. We compared only lipid variables, and did not take into account the current use of medication or the inflammatory
state of the patients. Since the commonly used statin and angiotensin enzyme inhibitors and angiotensin II receptor blockers
may alter the inflammatory state, they may weaken the relationship between total cholesterol and LDL-cholesterol and the extent
of coronary disease. This is because they act more on LDL-cholesterol and less on HDL-cholesterol and triglycerides.
Nearly all routinely assessed lipid variables were associated with the extent of coronary disease, but only the
ratio of triglycerides to HDL-cholesterol or to HDL-c were robustly associated with disease extent. Elevation in the ratio
of TG to HDL-c was the single most powerful predictor of extensive coronary heart disease among all the lipid variables examined.
1. Miller NE. Associations of high-density lipoprotein subclasses and apolipoproteins with ischemic heart disease
and coronary atherosclerosis. Am Heart J. 1987;113:589–97.
2. Robinson D, Ferns GA, Bevan EA, Stocks J, Williams PT, Galton DJ. High density lipoprotein subfractions and
coronary risk factors in normal men. Arteriosclerosis. 1987;7:341–6.
3. Williams PT, Krauss RM, Vranizan KM, Stefanick ML, Wood PDS, Lindgren FT. Associations of lipoproteins and
apolipoproteins with gradient gel electrophoresis estimates of high density lipoprotein subfractions in men and women. Arterioscler Thromb. 1992;12:332–40. [PubMed]
4. Hanak V, Munoz J, Teaque J, Stanley A, Jr, Bittner V. Accuracy of the triglyceride to high-density lipoprotein
cholesterol ratio for prediction of the low-density lipoprotein phenotype B. Am J Cardiol. 2004;94:219–22. [PubMed]
5. Da luz PL, Cesena FH, Favarato D, Cerqueira ES. Comparison of serum lipid values in patients with coronary
artery disease at <50, 50 to 59, 60 to 69, and >70 years of age. Am J Cardiol. 2005;96:1640–3. [PubMed]
6. Rinqqvist I, Fisher LD, Mock M, Davis KB, Wedel H, Chaitman BR, et al. The Coronary Artery Surgery Study. Prognostic
Value of Angiographic Indices of Coronary Artery Disease from the Coronary Artery Surgery Study (CASS) J
Clin Invest. 1983;71:1854–66. [PMC free article] [PubMed]
7. Krauss RM, Burke DJ. Identification of multiple subclasses of plasma low density lipoprotein in normal humans.
J Lipid Res. 1982;23:97–104. [PubMed]
8. Scheffer PG, Bakker SJL, Heine RJ, Teerlink T. Measurement of LDL particle size in whole plasma and serum by
high performance gel-filtration chromatography using a fluorescent lipid probe. Clin Chem. 1998;44:2148–51. [PubMed]
9. Kuller L, Arnold A, Tracy R, Otvos J, Burke G, Psaty B, et al. Nuclear Magnetic Resonance Spectroscopy of Lipoproteins
and Risk of Coronary Heart Disease in the Cardiovascular Health Study. Arterioscler Thromb Vasc
Biol. 2002;22:1175–80. [PubMed]
10. Ballantyne CM, Hoogeveen RC. Role of lipid and lipotrotein profiles in risk assessment and therapy. Am Heart J. 2003;146:227–33. [PubMed]
11. Hong MK, Romm PA, Reagan K, Green CE, Rackley CE. Usefulness of the total cholesterol to high density lipoprotein
cholesterol ratio in predicting angiographic coronary disease in women. Am J Cardiol. 1991;68:1646–50. [PubMed]
12. Castelli WP, Anderson K, Wilson PW, Levy D. Lipids and risk of coronary heart disease. The Framingham Study.
Ann Epidemiol. 1992;2:23–8. [PubMed]
13. Manninen V, Tenkanen L, Koshinen P, Huttunen JK, Manttari M, Heinonen PO, et al. Join effects of serum triglycerides
and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Sudy. Implications
for treatment. Circulation. 1992;85:37–45. [PubMed]
14. Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, et al. Effect of potentially modifiable risk factors
associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet.
15. Gotto AM, Jr, Whitney E, Stein EA, Shapiro DR, Clearfield, Weis S, et al. Relation between baseline and on-treatment
lipid parameters and first acute major coronary event in the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/Tex
CAPS) Circulation. 2000;101:477–84. [PubMed]
16. Walldius G, Jungner I, Holme I, Astveit AH, Kolar W, Steiner E. High apoliprotein B, low apolipoprotein A-I,
and improvement in the prediction of fatal myocardial infarction (AMORIS Study): a prospective study. Lancet.
17. Gaziano JM, Hennekens CH, O’Donnell CJ, Breslow JL, Buring JE. Fasting triglycerides, high density lipoprotein,
and risk of myocardial infarction. Circulation. 1997;96:2520–5.
18. Jeppesen J, Hein HO, Suadicani P, Gyntelberg F. Triglycerides concentration and ischemic heart disease: an
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Articles from Clinics are provided
here courtesy of Hospital das Clinicas da Faculdade de Medicina da Universidade de Sao Paulo
May 16, 2011 | By
High levels of triglycerides in your bloodstream put you at risk for heart attacks and
strokes. Diet and lifestyle affect the amount of triglycerides stored in your fat cells. High-density lipoprotein, also known
as the "good" cholesterol, helps your body eliminate triglycerides. Improve your heart health by maintaining a healthy balance--ratio--between
triglycerides and HDL cholesterol.
You want to keep your triglycerides low and your HDL cholesterol high. Triglyceride levels
below 150mg/dl--milligrams per deciliter of blood--and HDL cholesterol above 60 mg/dl rank as healthy. Aim to keep your triglycerides
below 100mg/dl for optimal heart health, according to the American Heart Association. Triglycerides that measure more than
200mg/dl put you at high risk of heart attack and levels above 500mg/dl put you at very high risk. Women face additional cardiovascular
health risks if their HDL cholesterol falls below 50mg/dl, men if below 40mg/dl.
Strive for a triglyceride-HDL ratio of less than 2:l. This means that your triglycerides
should not total more than twice your HDL cholesterol. If your triglycerides measure 100mg/dl and your HDL cholesterol is
50mg/dl, this would give you a 2:1 ratio--100 divided by 50 equals 2. Higher ratios signal potential for heart problems. A
4:1 ratio is high and a 6:1 is very high. If your triglycerides measure 200mg/dl and your HDL cholesterol is 50mg/dl, this
would give you a 4:1 ratio. Triglyceride levels of 300mg/dl and an HDL of 50md/dl provides a 6:1 ratio.
Your HDL cholesterol scavenges your bloodstream for triglycerides and low-density lipoprotein,
LDL or "bad" cholesterol. It removes as many triglyceride and LDL cholesterol deposits as it can and ships them to your liver
for disposal. But your HDL cholesterol can't function properly when the ratio of triglycerides to HDL moves beyond 2:1. When
your HDL cholesterol becomes greatly outnumbered by triglycerides, your risk of developing cardiovascular disease increases.
Diet and exercise can help you achieve a healthy balance.
The American Heart Association recommends a triglyceride-lowering diet that limits consumption
of saturated fat to 16g a day and trans fat to 2g daily. The AHA diet also restricts calories obtained from foods with added
sugar to 100 per day for women and 150 per day for men. Adding exercise can help lower your triglycerides and boost your HDL
cholesterol. Aim to include 150 minutes of moderate exercise in your weekly routine. Brisk walking counts as moderate exercise.