ART heart attack and stroke part 2

Boomers Health – Disease Prevention Series

Heart Attack and Stroke

Part II


Good Cholesterol, Bad Cholesterol and Heart Attack Risk

3D illustration of Heart - Part of Human Organic.

Glenn Sargent

For Boomers Health

© Copyright Boomers Club Pty Ltd June 2016


Part 1 of this series described that fats and cholesterol don’t mix with blood and the bodies solution is to wrap them up in particles called Lipoproteins. I Part 2 Lipoproteins are explained, along with the measurements of them your GP will request when we get our annual checkup.  And finally what to ask you GP for to help him / her obtain more accurate and useful information upon which to give appropriate advice.


There are three basic types of these Lipoprotein particles. One are called Chylomicrons, which are made by our intestinal cells to deal with the fats and cholesterol we eat (plus cholesterol produced by the liver in bile salts). Two other Lipoproteins are manufactured by the liver. The first is called Very Low Density Lipoprotein (VLDL) which delivers fats to fat tissue and cholesterol to cells that need it. Thirdly there is High Density Lipoprotein (HDL). Also manufactured by the liver HDL removes unwanted cellular cholesterol from tissues from tissues.

All these Lipoproteins undergo change as they take up, deliver or transfer their contents, once degraded all three Lipoprotein remnants are returned to the liver for reprocessing, and the leftovers are excreted.  These two types of Lipoproteins are called High Density Lipoprotein (HDL) and Very Low Density Lipoprotein (VLDL).

When these Lipoprotein particles and their contents infiltrate the artery walls CAD results and increases the risk of heart attack and stroke. How and why this occurs will be addressed later.


Your GP, as part of regular checkups will order blood tests to be done to make sure everything is working properly. In essence the earlier anything wrong is discovered the better the chance of the issue being fixed. As part of the test the GP will request a lipid profile to help determine the risk heart attack and stroke.  This test will measure HDLc, Total Cholesterol and Triglycerides. Triglycerides are forms of fat.  From this LDLc is calculated, NOT measured.

What is LDLc and HDLc?

There are different types of HDLc some good some bad, but generally mostly good. These different types of HDLc can be measured accurately but measurement is complex and relatively expensive.

Furthermore, knowing your different types may be of little personal benefit. In order to measure the amount of HDLc quickly and cheaply the amount of cholesterol carried by HDL is measured, and this called HDLc or “good cholesterol”. The total amount of Triglycerides (fats) and the Total amount of Cholesterol is measured, from these LDLc (bad cholesterol) is calculated. As VLDL delivers its contents it decreases in size and becomes more dense passing through stages one of which is Low Density Lipoprotein LDL. By estimating cholesterol content the amount of LDLc is calculated and is otherwise known as “bad cholesterol”.



We have all been led to believe that if we can increase “Good Cholesterol” and decrease “Bad Cholesterol” the risk of heart attack will be reduced.

A new drug has been developed called a CETP inhibitor which promised to both raise the good and lower the bad, a cardiologist’s dream drug. The big drug companies have had a few goes but failed either due to unacceptable side effects or poor performance; that is they did not raise the good and lower the bad to the extent expected. Finally Eli Lilly (a major pharmaceutical company) developed a CETP inhibitor that found the holy grail; it substantially increased good cholesterol and at the same time substantially decreased bad cholesterol, without producing unacceptable side effects; it worked!

But before the drug could be marketed it required USA Food and Drug Administration approval and it had to put the drug through a proper clinical trial.

The trial included 12,000 people, 6000 taking the drug and 6000 in a control group, the trial was extended for an extra year and a half and eventually abandoned by Eli Lilly. The reason for the abandonment stated by the company was “futility”. Simply put there was no difference in the number of heart incidents between the two groups. Even though the drug performed better than any other to alter HDLc and LDLc, it had absolutely no effect on heart attack risk.  So in this case good and bad cholesterol didn’t matter.

On the other hand we have a class of drugs called Statins which lower LDLc and they have been shown to reduce the risk of heart attack by about 30%.  In essence this means they work for about 30% of the people who take them and fail for 70% of the people who take them.

Why do Statins only work for 30% (between 16% and 45% depending on research design) percent of patients and CETP inhibitors work for no one?  This is an important question because this fact provides important clues to the to the relationship between heart attacks and “cholesterol” readings.


Our liver makes Very Low Density Lipoprotein (VLDL) particles. They are relatively large particles full of fats and cholesterol.  As time passes the fats and some cholesterol are transferred to the cells, and the VLDL also interacts with the HDL.

As this happens particles become smaller and denser. VLDL, becomes IDL, which becomes LDL, which becomes SDLDL (small dense LDL particles). It is now known that Coronary Artery Disease (CAD) is “accelerated” by these very small particles entering the artery wall. Firstly, because they may be small enough to squeeze between the cells that line the interior of the arteries and secondly, because they stay in the circulation for longer.

This means they are more likely to become damaged or oxidised which may in turn affect or damage the lining of an artery making it more permeable and susceptible to invasion by SDLDL.

In 1985 two researchers, Goldstein and Brown, won the Nobel prize for medicine for their discovery of why Statin drugs actually worked. Statins had the effect of increasing the number and efficiency of LDL receptors located on liver cells.

These receptors are responsible for taking LDL from the blood stream and repackaging the contents into fresh new large (safe and good) VLDL particles. When the number and efficiency of LDL receptors is increased the LDL particles spend less time in circulation and therefore have less time to become the dangerous small dense LDL particles that are associated with with the type of CAD that can result in heart attacks.  So do you have the dangerous small dense LDL particles?

The answer is you don’t because your GP does not tell you about the test and explain its benefits, and  / or, because it’s not on the medicare benefits list and you have to pay for it ($76 at the time of writing). Or possibly because they may not know it is available to the public.  Just let your GP know you want the test and ask for the script.


The standard lipid profile testing does not give your GP the information needed to make a fully informed decision with regard to the advice given.  Two people with exactly the same level of bad cholesterol (LDL) recorded by the standard test can have dramatically different heart attack risk and outcomes.  Check the results of these two LDLc subfraction tests.

The red represents the small dense LDL particles that modern research believes are highly atherogenic (dangerous CAD).  It should be noted the sum total LDL in the first chart is 104 mg/dl (2.8/mm/l) and the second is 109 mg/dl (2.7mm/l); that is no measurable difference?  At the bottom of each report the patient is classified as either Type A or Type B.  Type A indicates we can sleep rather easily. Type B means we should do something about it, STRAIGHT AWAY, see your GP again!!

Much of the above has been about bad cholesterol (LDL) since it is the main focus of practitioners but what about about good cholesterol (HDL).  High HDLc is associated with a lower risk of coronary artery disease and by implication a lower risk of heart attack and stroke.

Thus raising HDL should decrease the risk of heart attack and stroke.  While it “appears” that high good cholesterol is beneficial, artificially raising Good Cholesterol with medicines like like Niacin, and Fenofibrates will, according to the clinical studies, be of little or no benefit if one is already prescribed a Statin. Here it gets tricky because even though these medicines can raise good cholesterol the evidence is that they do not further reduce the risk of heart attack and stroke compared to taking a Statin alone.  This is especially so where Triglycerides (Fat) are high and HDLc low. This is a discussion you should have with your GP.

Most importantly; it appears that how much “good cholesterol” we need is relative to how high our Triglycerides are.

TRIGLYCERIDES (A fancy name for fats)

Triglycerides are possibly the most important component of the standard blood test.

Why So?

Cholesterol levels are controlled by internal signalling systems. In essence if we eat it the liver makes less and vice versa. Essentially cholesterol levels are not generally affected by the amount of cholesterol we eat.

There are no such balance controls for fats.  There is no limit as to the amount of fat we can eat or our liver can make. If we eat fats they are packaged up into chylomicrons. If we overeat anything, fats, carbs, protein or alcohol the excess is converted to fat (Triglycerides) and packaged into VLDL particles, which become IDL, LDL, and SDLDL (the bad guys). So high triglycerides and hence CAD accelerating SDLDL and Chylomicron remnants are directly related to how much and what we eat, except for one thing, cholesterol.  It doesn’t really matter much how much cholesterol we eat, where do these fats end up?  Have a look in the mirror!  Oh and also into our artery wall.

Having said this it is very important to note that the vast majority of overweight Australians are probably “fat” not through eating fat, but simply from eating too much, especially refined carbs and sugars.  Remember, all excess food gets converted to fat by the liver!

Triglycerides are the most important reading on our lipid profile test, because we can control them by how much and what we eat. Less consumption means fewer SDLDL particles and a reduced requirement for high HDL levels!!!!!!!

Considering that LDL particles have a half life of 4 to 5 days and Small Dense LDL roughly the same then the result of beneficial dietary change (energy intake) should be evident within 30 days.

Note while cholesterol levels are harder to change, the benefits of Good Cholesterol are enhanced as Triglyceride levels are reduced. Live lean to live long.


It’s a big word “Apolipoprotein”, can you say it? The medical scientists just write “Apo” when referring to them.  We have discussed Lipoproteins above. On the outer shell of the lipoprotein particles are proteins that are “signalling” Apo’s. They determine what type of particle it is and what the that particle is programmed to do. Some Apo’s manage how the different lipoproteins interact with each other and the cells in our tissues, in particular ApoE. There are three types of this ApoE, and each of us carry two of them, one from each of our parents. By themselves they are called ApoE2, ApoE3 and ApoE4. Because we obtain them genetically from both our parents an individual could be ApoE2,3 or E2,4 or E2,2 or E4,4 or E3,3 and so on. There are a large number of permutations.

When it comes to heart attack and heart disease risk, personal ApoE type plays a substantial role in the risk of heart attack as do some other apolipoproteins. In essence the risk of CAD and Heart attack is highly individual. A very few of us will be at extremely high risk or at extremely low risk and the rest somewhere in the middle.

A practitioner using “good and bad cholesterol” numbers to determine risk and hence the medication or lifestyle advice given is akin to a blind man trying to shoot a black cat in a dark room. About 20% of sudden heart deaths occur in people who have perfectly good “bad cholesterol” profiles. This is why it is so much better to obtain LDL subfraction test results, and to keep using them to find out what treatment works best for you.

Should we be tested for ApoE types?

Personally I’m not sure if I would want to know, nor do I know if it can be done outside a research laboratory. The fact is we can’t change the genetics we have inherited and we all owe it to ourselves and society in general to stay well no matter what our personal genetic risk is, and whatever that risk may be it just makes common sense to take simple practical steps to minimise the risk and extend vital healthy life. What we can do with food and lifestyle to reduce risk is covered in Part IV.


Numerous food products (and some supplements) are available that have added plant sterols (phytosterols) and advertise that consumption of the product reduces cholesterol. These are usually margarines, yoghurts and milk products with brand names you may be familiar with. Pro-Activ is probably the most visible brand. Here Boomers Health takes a very strong stance, don’t buy them, don’t consume them, EVER EVER. Goto for more info.


Plaque (cholesterol and fats) that builds up in our Artery walls is not the cause of heart disease, it is the result of it and may end up resulting in a heart or stroke or both.

Cholesterol testing (the lipid panel test) is an indicator of heart heart and stroke risk.  Low “triglycerides” and high “good cholesterol” is an anti-atherogenic (safest) lipid profile so long as the “bad cholesterol” sub-fraction test is clear of small dense “bad cholesterol” particles.

Once men reach age forty and women age fifty a lipid panel test should be carried out including the LDLc sub-fractions. Demand your GP has the results sent to you as well as themselves. If they will not consider changing your GP,  you need these records to monitor change, seek second opinions etcetera.

The LDLc sub-fraction test is not covered under the Pharmaceutical Benefits Scheme and therefore it has to be paid for.  At the time of writing the best price (~$76) we can find from a credible pathology laboratory is from Adventist pathology which is now owned by Sonic health care.  Hence any pathology centre operated by Sonic can get the test done.  For example, in Melbourne that is Melbourne Pathology.  You will need a script, all your GP has to do is request an “LDLc Subfraction Test and direct you to a Sonic owned centre.