An extract from – Good Fat Bad Fat & the HeartStopper Gene
by Matthew J Bayan (publishers – Simon & Schuster)

AT forty five, Matthew J. Bayan appeared to be in robust health. He exercised daily, ate a low-fat diet, never smoked and avoided excess stress.

But early one morning, he was jolted awake by a massive heart attack. Rushed to a nearby hospital, Bayan was close to death.

In fact, he did die – doctors restarted his heart more than 70 times.

As he recovered, Bayan received the usual treatment for heart patients, which included a very low-fat diet-one that Bayan followed faithfully.

But to Bayan’s and his doctors’ growing concern, his bad-cholesterol and triglyceride levels worsened on the very low-fat diet. Something was wrong.

What Bayan discovered was that he carried the apolipoprotein B gene, a gene that could destroy his heart by triggering his system to produce more bad cholesterol on a very low-fat diet than on a diet higher in certain kinds of fat.

Bayan also discovered that not only has he this killer mutation, which he dubbed the ‘HeartStopper gene’, but that an estimated 20 per cent of the population carries this gene as well – and the vast majority doesn’t even know it!

Are You At Risk Of The HeartStopper Effect ?

This quiz will help you determine if you might have the HeartStopper Effect, a genetic defect that triggers your system to create more bad cholesterol than it should.

Answer as many of these as you can, and then add up your score.

Has a direct relative (parent, grandparent, uncle, aunt, brother, sister) had a heart attack?
• Score 75 for yes. ________

Has any direct relative had a stroke?
• Score 75 for yes. ________

Were any of them younger than fifty-five when they had a heart-attack or stroke?
• Score 50 for yes. ________

Are you overweight or do you smoke?
• Score 20 for yes. ________

Is your total cholesterol over 5.0 mmol/L?
• Score 20 for yes. ________

Is your HDL under 1.0 mmol/L (male) or 1.3 mmol/L (female)?
• Score 30 for yes. ________

Is your LDL over 3.4 mmol/L?
• Score 20 for yes. ________

Are your triglycerides over 3.5 mmol/L?
• Score 20 for yes. ________

Divide your total cholesterol by your HDL. Is the answer over 5?
• Score 50 for yes. ________

TOTAL ________
Now, Add Up Your Points …

• If you scored over 100:
You are in Moderate Danger of a Heart Attack.

• If you scored over 150:
You are in Serious Danger of a Heart Attack.

• If you scored over 200:
You are in Extreme Danger of a Heart Attack


Cholesterol is a complex lipid or fat compound. Cholesterol does not float through the blood all by itself. To move around in the body, it must be linked to protein, hence the term lipoprotein. This package of protein and fat moves through the blood to supply cells with fat. In a normal transaction, a lipoprotein bumps up against a cell’s outer membrane and the cell absorbs the fat. However, for someone with the HeartStopper Effect, the lipoprotein we call apolipoprotein B, for instance, does not perform in a normal way. ApoB moves into arterial walls 40 percent faster than other lipoproteins. Once there, it is more likely to create dangerous, unstable plaque.

What is this stuff called plaque? How does it form? Where does it come from?

Visualize a tube narrower than your little finger. Blood passes through that tube called a coronary artery to feed the heart muscle so it can pump blood to the rest of the body as well as itself Over time, tiny particles of cholesterol in the blood stick to the walls of the artery. These particles build up into what is called cholesterol plaque.

It appears we live almost all of our lives with plaque. Autopsies show that cholesterol plaque is found even in children. For the normal individual, this plaque builds slowly over decades, but never reaches a thickness sufficient to block an artery. For those who develop heart disease, the plaque grows more substantially, but also usually at a steady pace. For those with developing heart disease, this plaque thickens and eventually begins to block the flow of blood through the artery, causing angina pectoris, chest pain.

Angina usually starts in one’s late fifties and is usually brought on by exertion. If insufficient blood flows through one of the arteries to the heart, the part of the heart that is fed by that artery begins to get starved for oxygen. If the afflicted person relaxes and reduces the load on the heart, the pain goes away. For those with chronic angina, a prescription of nitroglycerin is used to provide temporary relief by causing coronary arteries to dilate, allowing more blood to flow. Other symptoms of clogged arteries are shortness of breath and dizziness.

If the plaque blockage of an artery increases to where the artery cannot carry sufficient blood to the heart for a prolonged period, that part of the heart fed by the blocked artery begins to die. This is a heart attack. In normal heart disease cases, angina symptoms usually start slowly and increase over time, giving warnings along the way.

By the time we are adults, almost every person has some arterial plaque. Such blockage is not considered serious until it reaches approximately 70 percent closure of the artery. Prior to that, there is sufficient blood to supply the heart’s needs, even during exercise. However, with blockage above 70 percent, the flow of blood is too restricted; the heart muscle becomes oxygen-starved and pain results. Eventually, total blockage can occur.

Depending on which artery or arteries this blockage occurs in, the impact on the heart will vary. Total blockage of some of the minor arteries can cause discomfort or mild heart attacks, but afterward, the patient is able to function fairly normally. In my case, the artery being blocked was a crucial one-the left anterior descending artery (called the LAD), definitely not one you can easily live without. It feeds the front wall of the left ventricle, the part of the heart that gives blood the final big push as it leaves the heart.

Doctors now have options for treating arterial blockage, the most common being angioplasty and, for advanced cases, coronary bypass surgery.

After the angioplasty balloon pushes the cholesterol plaque against the arterial wall, the site of the original blockage may not continue to stay clear. In about a third of angioplasty cases, the artery does not respond well to being stretched outward. It constricts again to its previous shape, usually within a few months. Doctors will then recommend insertion of a stent to keep the artery open. A stent is a small stiff tube made of a screen-like material. its support inside the artery keeps the artery from closing down. It sounds crude, but it works.

With angioplasty and stents, all the surgical work is done inside the body using various tools that are worked into place within coronary arteries through incisions in the femoral arteries in one’s legs. Bypass surgery, however, is major surgery. The chest is ‘cracked’ by cutting open the sternum and spreading apart one’s ribs. The heart is exposed. Surgeons construct detours around clogged sections of coronary arteries by sewing in segments of veins they have cut from elsewhere (usually the patient’s legs). After coronary bypass surgery, it takes months for the patient’s wounds to heal and for bones in the chest to knit.

The problem with these approaches is that if the patient does not have a healthy diet and does not change behavior, plaque will continue to grow, and eventually these same sites will clog again, along with new sites. How often do you want your chest cracked? How often can you survive major surgery?

For most people, arterial blockage occurs over a long time and never exceeds 70 percent. They go their whole lives without heart problems. Plenty of people on high-fat, high-sugar diets are couch potatoes, smoke, and have high-stress jobs, yet they never get angina and never have a heart attack.

Then there’s the group that has the HeartStopper Effect. Recent research shows that roughly 25 to 30 percent of adults carry HeartStopper genes. Genetic mutations that negatively affect blood chemistry are evident in 80 percent of patients with coronary artery disease. For us, there is no long, gradual buildup of plaque into our sixties and seventies. For us, the timetable is accelerated; plaque can build at an alarming rate, regardless of our stress levels, our diets, or our physical conditioning. For us, the tiny particles of cholesterol are abundant and sticky. They cling to arteries in a mad race to destroy us. And for us, there is an added twist. We don’t grow the same plaque as everybody else.


In a normal individual, stable plaque builds up slowly and becomes a danger only when it threatens to close down a coronary artery. Unstable plaque, on the other hand, is dangerous no matter how much of it is present because it has the potential to tear and create a sudden blood clot.

These different characteristics of plaque are determined by the amount and type of cholesterol floating in the blood. In simple terms, when blood triglyceride and LDL cholesterol levels are high, plaque is gooey and unstable as it grows. When blood triglyceride and LDL cholesterol levels are low, the plaque becomes tougher, less mobile.

How can we deal with this? If we starve unstable plaque of its building blocks, it shrinks against the artery walls. It tightens up and becomes tougher. It is far less likely to rupture.

So, to treat the effects of the killer genes, it’s necessary to deal not only with the existence of plaque, but also its composition.

All plaque is a combination of fats and proteins that create a new interior wall inside an artery. A fibrous protein cap grows over the surface of stable plaque and holds it together. Stable plaque is the type of plaque that both normal individuals as well as the majority of heart disease patients grow.

Unstable plaque grows more quickly. The fibrous cap that grows over and protects normal plaque is not fully present in unstable plaque, leaving it open to damage. Think of the difference in consistency between peanut butter and honey. Stable plaque is more like peanut butter; unstable plaque is more like honey. Unstable plaque is more susceptible to movement of the body, to blood pressure changes, and to changes in the volume of blood passing through the artery. Pieces of unstable plaque can break off; it can crack or rip. This is because it is less tough than stable plaque and because the protective protein cap is only partially present or not present at all.

When unstable plaque rips or cracks, the platelets within the blood senses a break in the blood vessel and clotting occurs at the scene of the wound. However, in this case there is no wound, no breakage in the artery; there is only a breakage in the plaque wall. A small clot usually forms, breaks down, and dissolves without blocking an artery. However, a big tear can cause a big clot and a sudden, totally unexpected heart attack.

And guess what? When unstable plaque is involved, a heart attack can occur long before blockage of a cardiac artery reaches 70 percent, long before there is any warning from chest pain.

How Can This Happen?

Take my case. Dr Rough used an angiogram to actually look at my arteries from the outside through the use of real-time X rays. The artery that caused my heart attack was totally blocked. Not by plaque, but by a blood clot. Once he cleared the clot, he saw that the original plaque blockage was only about 40 percent, not enough to cause an MI or the warning of chest pain.

So, what had happened? The consensus in my case is that the unstable plaque coating on the walls of the artery actually ripped as a piece of plaque broke free. Blood platelets passing over the site interpreted this as a break in the wall of the artery and began clotting to repair the breakage. The clotting continued until the artery was totally blocked and the MI resulted.

The good news is that it’s possible to manage this deadly plaque. The bad news is that first you have to know you have the problem. Let’s look at the basic mechanisms that are manipulated by this disease as it forms unstable plaque.


Cholesterol is a building-block molecule that the body uses to produce all sorts of other substances such as vitamin D and steroids. We’ve all heard of steroids in reference to muscle building in athletes. But many more steroids are produced in our bodies, all made from cholesterol. For example, three of the most important human steroids are testosterone, the male sex hormone; progesterone, a female sex hormone; and oestrogen, the hormone that regulates a woman’s reproductive cycle. Without these three steroids there would be no sex drive, no sex, and no reproduction. The human race would perish if we could truly become cholesterol free. So, the advertising media’s campaign to make us think we need to eliminate cholesterol is misinformation.

We’re inundated with information about cholesterol all the time. It’s become conventional wisdom to limit our intake of cholesterol. Almost every food package now shows the cholesterol content per serving to help us in this task. But what’s important about cholesterol is not so much the amounts in the foods we eat as how much of it winds up in our bloodstreams.

Cholesterol is a fat compound that we can ingest or that our bodies can produce. You can starve your body for fat-eat no fat at all-and you will still have cholesterol in your blood. The human body is a complex chemistry set. It will break down carbohydrates and proteins and build cholesterol from the ground up if it has to. We cannot stop this process.

Considering the media bombardment of the past two decades, cholesterol has become equal to kryptonite in our perceptions. We hear terms like ‘good’ cholesterol and ‘bad’ cholesterol as we strive to exclude all cholesterol from our diets and our bodies. But cholesterol is not an optional food ingredient. It is an essential component basic to the functioning of the human body.

There are two main types of cholesterol: good and bad. The good cholesterol is called HDL for high density lipoproteins; the bad cholesterol is LDL for low density lipoproteins. (A lipid is a fatty acid; it is the building block of more complex forms of fat. Where you see lipid, just think ‘simple fat.’ When a lipid is attached to a protein, it is called a lipoprotein.)

HDLs and LDLs engage in a constant tug-of-war within our bodies. The low density lipids are the dangerous ones that attach themselves to the walls of arteries, build up, and choke off the blood flow. This causes chest pain and eventually a heart attack. The high density lipids are the beneficial ones; they actually go out and ‘grab’ LDL particles and carry them away from artery walls and back to the liver for disposal. They are like scrubbers. They keep the arterial system clean. Otherwise, we’d all clog up rather quickly.

For a healthy heart and circulation system, HDLs and LDLs must be in balance. There must be enough HDLs to keep the LDLs under control. The killing mechanism of the HeartStopper Effect is to throw off this balance-to allow the LDLs to overcome the HDLs and to build up unstable plaque in coronary arteries.

How does the gene do this? Another brief chemistry lesson. LDLs come in three forms: large-particle, intermediate-particle, and small-particle. Large LDL particles are easy for the HDLs, the scrubbers, to grab and to move around. It’s the small-particle LDLs that are dangerous. HDLs have a tough time grabbing them. (It’s like the difference between catching a softball versus a golf ball.) Consequently, the small particles build up in coronary arteries almost unimpeded.

The HeartStopper Effect stimulates the body to produce more small-particle LDLs. Then, to be extra lethal, it also suppresses production of HDLs. So, not only does the HeartStopper Effect load up the body with the worst building blocks for unstable plaque, it also reduces the body’s ability to move these building blocks away from artery walls. Double Whammy!!


Triglycerides are simple fatty molecules. They are like building blocks for other, more complex fat compounds such as cholesterol. Unlike cholesterol, which takes weeks and months to increase or decrease in the body, triglycerides increase or decrease in a matter of days. Their existence in the blood is very much influenced by sugar and alcohol consumption.

Triglycerides play the trigger role in crossing over from large-particle LDL production to small-particle production. When triglycerides are abundant in the bloodstream, they provide the building blocks the HeartStopper needs to increase small-particle production. This crossover point appears to be when triglycerides exceed approximately 3.5 to 4.0 mmol/L.

• If one produces large amounts of small-particle LDL, one is classified LDL Type B or LDL Subpattern B.
• If one produces mostly large-particle LDL, one is classified as Type A or Subpattern A (normal).
• One who produces both is Intermediate.

Generally, in normal individuals the production of small-particle LDL is less than 15 percent of total LDL.

In carriers of a killer gene, small-particle LDL production can rise to 35 percent, 40 percent, and higher. Being Type B all by itself constitutes a threefold heart risk.

Because triglyceride levels can fluctuate rapidly, it does not take much candy and brownies or alcohol or fast-food bingeing to cross over into small-particle production. This crossover can happen in a matter of days.

Triglyceride levels in the blood directly affect the production of LDLs. High triglyceride levels increase production of LDLs, low triglyceride levels decrease production. One can see that managing triglyceride levels not only affects total LDL production, but also is effective in managing the Type A/Type B crossover. Diet and drug therapy can beneficially use this crossover point.

So, theoretically, by starving the body of triglycerides, by staying below the crossover point, we should be able to decrease the building blocks necessary for small-particle LDL production. In normal people this is true. The problem is that for those of us afflicted with the HeartStopper Effect, triglyceride levels tend to stay high, no matter what we eat.


So, now we have seen that cholesterol comes in two flavors: HDL and LDL.

• We’ve seen that LDL can be small-, medium-, or large-particle.

• We’ve seen that plaque can be either stable or unstable.

• And we’ve seen that triglycerides are the enablers that affect small-particle LDL production.

What do we do with this information?

Unfortunately, we have been conditioned over the past two decades to look at cholesterol simplistically. When we get tested for blood cholesterol levels, we’re usually given total cholesterol counts. This is misleading for those with a heart-killer gene.

Total cholesterol measures just that, all the cholesterol in the blood. It does not distinguish between HDL and LDL levels. The American Heart Association and most doctors will counsel that a total cholesterol level less than 5.0 mmol/L is best. Over 5.0 mmol/L is riskier as the level rises. It is generally accepted that as the level approaches 7.75 mmol/L or higher, one is in great danger.

However, if we only use total cholesterol as our indicator (as is the case in general health checkups given by general practitioners), we are completely uninformed about the existence of the HeartStopper Effect. For example, someone could have cholesterol of 5.0 mmol/L and be told by his doctor he’s in great shape. But he could have a high small-particle LDL count and his body could be building up arterial plaque at a hellacious rate. He leaves the doctor’s office feeling confident, and six months later he’s dead.

This is more likely than you might think; 80 percent of people with coronary artery disease do not have elevated cholesterol levels. So, a total cholesterol count is only effective in finding an abnormally high cholesterol level, which requires immediate treatment; it is virtually worthless as a diagnostic for many people with either straightforward heart disease or the HeartStopper Effect.

How many people leave their doctor’s office certain that they are okay, when in fact they carry the seeds of sudden death in their chests?

The first step to finding out if you have the HeartStopper Effect or any other kind of coronary artery disease is to get what’s called a lipid panel. Unfortunately, most doctors usually don’t order this test unless one’s total cholesterol is already high. This blood test breaks down total cholesterol and shows HDL and LDL levels as well as triglyceride levels. These are essential numbers for beginning diagnosis only, because even a lipid panel is not a conclusive indicator for carriers of a HeartStopper gene.

Many carriers have lipid panel results that are completely normal, completely misleading about what is going on deeper down in their blood chemistry. But let’s use the lipid panel for now because it is cheap, widely available, and is valuable for managing health status in other types of heart disease patients and in the population in general.

Let’s use the above example again. A forty-year-old man has total cholesterol of 5.0 mmol/L. But his HDL is 0.8 mmol/L and his LDL is 4.5 mmol/L. His triglyceride level is 6.5 mmol/L. His HDL is too low to stop plaque buildup. The ratio of total cholesterol to HDL is 6.25 (divide total cholesterol by HDL), a time bomb.

But remember, his total cholesterol is 5.0 mmol/L, within the commonly accepted healthy range. If we relied only on a test of total cholesterol, we would completely miss the underlying problem.

To be clear, for most people concerned about their health, a total cholesterol level less than 5.0 mmol/L is usually considered healthy. By far, this is the majority. But how do you know if you are part of the ‘normal’ majority or a carrier of a heart-killer gene? If you have the HeartStopper Effect, ignorance can be fatal.

Knowledge of the HeartStopper Effect is actually quite advanced. Viable treatments exist. The problem is that many cardiologists are not primed to look for the special genetic signals. In the great wave of heart patients that washes over doctors every year, it’s tough to spot those who have killer genes versus those who have bad blood chemistry because of lousy diets, lack of exercise, and too much alcohol, stress, and smoking.

Those of us who carry these genes get lumped in with the rest. This is dangerous. I’m an example of how this can happen.

Following my heart attack, my doctors highly recommended that I enroll in a course of treatment developed by Dr Dean Ornish. This treatment plan consists of three elements: radically low-fat diet, stress management and promotion of emotional well-being, and aerobic exercise. In all, it’s a well-thought-out plan of treatment. Dr Ornish has achieved some startling reversals of cardiac artery blockage. He has turned the conventional wisdom about heart disease treatment on its ear.

The most controversial part of what has become known as the Ornish Diet is its nearly no-fat basis. For many patients, this is a difficult bridge to cross, but for those who make it, eating almost no fat becomes a religion. These folks are the Greenpeace of the cardiac community.

I tried the Ornish Diet and I think it has merit for the majority of cardiac patients. The problem was that in my case it could have proven to be dangerous. Killer genes and a no fat diet don’t mix. On the surface, this seems illogical, inconsistent. If fat causes cholesterol and cholesterol builds up as arterial plaque, then cutting off the source of the problem should solve the problem, right? Not so fast.

First of all, the body must have cholesterol to function. The body manufactures cholesterol no matter what we eat. It’s the quantity and composition of the cholesterol that are important.

But remember: successful treatment of the HeartStopper Effect rests on the need to keep HDL levels high and to keep the body from creating small particle LDLs.

For someone with the HeartStopper Effect, cutting out all or almost all fat from the diet causes the body to look for energy elsewhere. After all, the body has only three sources of energy and material: fats, proteins, and carbohydrates. If we take away fats, the body must find fat building blocks in proteins and carbohydrates. My first-hand experience with this phenomenon came when I restricted my fat intake to less than ten grams per day.

An ultralow fat diet for me could have been thirty grams of fat, so I was really being extreme. This was soon after my heart attack my cardiologist at the time did not know I carried a killer gene. He was perplexed that on such a fat restricted diet, my LDLs and triglycerides were rising. This was a counterintuitive result.

Several months later, after I consulted with a new cardiologist, he and his assistant finally determined that my body’s chemistry was doing an end run around my low fat, low sugar diet. My body was converting the carbohydrates that were now abundant as fat replacements in my diet oatmeal, corn, and pasta into sugars. This drove up my triglyceride levels, which allowed the killer gene to manufacture LDLs. By whatever means it took, this enemy gene was determined to clog my arteries and kill me.

Although he felt that the Ornish. Diet was good therapy for most cardiac patients, my cardiologist did not feel that Ornish’s approach was good for me or for those who have the HeartStopper Effect. Ornish’s approach attempts to correct coronary artery disease through nutrition and tries to avoid drugs unless absolutely necessary. Though I agreed with the philosophy of the Ornish Diet, I could not follow it.

To illustrate, my triglycerides pre Ornish were around 4.60 mmol/L moderately high; after a month on the Ornish Diet, my triglycerides shot up to an extremely high 10.72 mmol/L! Rather than using the ultra low fat approach of Ornish, I needed to augment my dieting efforts with cholesterol lowering drugs and pure sacrilege to Ornish – increased fat intake. My enemy was just too strong, too wily, too treacherous.

I am not alone in having an unexpected response to a low fat diet. This seeming anomaly is further illustrated in a 1994 study conducted by the Lawrence Berkeley Laboratory at the University of California. The study was designed to show the effects of a high fat diet versus a low fat diet on blood lipid levels.

The study focused specifically on how diet affects individuals with normal levels of small LDL particles (Type A) compared to those with high levels of small LDL particles (Type B).

Going from a high fat diet to a low fat diet lowered total cholesterol, HDL, LDL, and triglycerides for test subjects, but there was one unexpected result: none of the Type B subjects converted to Type A, but in the six week period of the test, 41 percent of the Type A group converted to Type B when they went on a low fat diet (in this case, 24 percent of calories).

Also, the drop in protective HDL for this converted group was greater than in the Type A subjects who remained Type A.

These results were on a diet with 24 percent of calories coming from fat. I would call such a diet moderately low fat. It’s when you get down below 10 percent of calories that you have a really low fat diet. The Ornish. Diet recommends fat intake of 10 percent of caloric intake.

If 41 percent of a randomly selected test group developed the dangerous small particle LDL syndrome by adopting a diet change that definitely was not drastic, how can cardiologists and nutritionists routinely recommend major reductions in fat intake without much more detailed analysis of a patient’s condition?

To really nail down this issue, consider this: The same University of California researchers repeated their study and reported findings in 1999. Instead of using a fat intake of 24 percent of calories as in the original study, they reduced fat intake to 10 percent of calories. In this study, 32 percent of the male subjects converted from normal Type A to the dangerous Type B LDL subclass in only ten days.

So, what if you’re not under a doctor’s care, are not at particular risk of heart disease, but just want to shed some extra kilos? Assuming your LDL is the normal Type A subclass, your new diet could convert you from normal risk to a triple heart attack risk in from ten days to six weeks. Without the diagnostic information provided by an LDL subclass test, you face huge risks even when you think you’re doing something good.

To be clear: If you reduce fat intake, in order to maintain calorie intake it is unavoidable to increase carbohydrate intake. The types of carbohydrates you eat have a large effect on the amount of triglycerides and small particle LDL your body will produce. Cake, cookies, candy, and other sugar-rich foods will cause a rapid increase in triglycerides, whereas vegetables, fruits, and grains won’t.

Depending on your fat intake, any carbohydrate, whether simple or complex, can be converted to triglycerides and then to small-particle LDL.

Carriers of a HeartStopper gene can counteract this process:
(a) by not adopting an ultra-low-fat diet
(b) by starting a doctor-supervised drug regimen
(c) by keeping consumption of saturated fats as low as possible
(and always below 7 percent of total calories).

It is essential for doctors to diagnose and treat each individual as an individual, rather than relying on the one-size-fits-all treatment paradigm that has for so long dominated cardiology and nutrition. It also shows that LDL subclass testing is essential for proper diagnosis and treatment of coronary artery disease.

Recent population studies show that 30 to 35 percent of adult males and 17 to 20 percent of adult females have small-particle LDL syndrome. These are numbers that cannot be ignored if proper, ethical care is to be given.


The interactions of total cholesterol, HDL/LDL mix, and triglycerides may seem complex. But the whole mix is manageable if one remembers some general rules.

• Most doctors would recommend that total cholesterol should be under 5.0 mmol/L; closer to 3.88 mmol/L would be better.

• Second, HDL should be around 1.16 mmol/L or above for males, 1.42 mmol/L or above for females; LDLs should be 2.6-3.9 mmol/L, preferably under 2.6 mmol/L.

• Third, triglycerides should be under 3.6 mmol/L for most people; for heart patients, under 2.6 mmol/L.

Can you be above or below these numbers?

Yes. These are targets, not absolutes.

Probably the single most important number is the HDL level.

Below 1.16 mmol/L is not good.

Above 1.29 mmol/L for males and 1.55 mmol/L for females seems to have a protective effect far beyond what one would expect.

Recent research has shown that people with high HDL level (1.80 – 2.32 mmol/L range) can have high cholesterol and yet do not seem to be prone to heart disease and tend to live into their nineties.

People with the HeartStopper Effect will not naturally have high HDL levels.

So, if you’ve recently had your cholesterol checked and you have very high HDLs, chances are that you are not going to have significant plaque buildup. You probably don’t have a heart-killer gene.