Despite the hype about cholesterol levels, 50% of heart attacks have normal readings prior to the catastrophic event.
CHOLESTEROL has such notoriety that whenever someone has a heart attack, it is always the first suspect. My friends come in all shapes and sizes, but two buddies come to mind.
The first is quite well endowed in the middle, eats what he sees, finds it hard to spare time for exercises, but is comforted by normal cholesterol levels. The other is mean and lean without an extra ounce of fat, watches his diet, runs marathons “part time”, and yet “suffers” from high cholesterol.
If I had to trade places, the choice would be the latter. Despite the hype about cholesterol levels, 50% of heart attacks have normal readings prior to the catastrophic event.
Progressive damage: Atherosclerosis is unavoidable but it is alarming when it happens prematurely as this accelerates the risk of dying unexpectedly and prematurely.
More than two decades ago, we classified risks of heart attack into major and minor. The three accepted major risk factors were, and still are, hypertension, high cholesterol, and smoking. Heart disease was the number one killer then. Today, medicine is making amazing advances with new drugs, diagnostic tools, and therapeutic techniques that have made old timers like myself obsolete. Yet, heart disease is still the chart topper in current-day mortality statistics.
At the risk of ruffling some feathers, diagnosis and treatment is like treating a sick tree with noxious chemical sprays on the leaves. Perhaps it may make good sense to nurture the roots before the tree becomes sick.
Quoting an article titled Are You Courting A Heart Attack by yours truly (Sunday Star, July 21, 1991), it was stated that “Death due to heart attacks will continue to rise for at least another decade before we can see the results of health education efforts. Awareness towards the importance of preventive health is rather limited, even among the ‘well-educated’ segment of our population. The prevailing attitude of ‘I don’t feel it, I don’t care’ should be discarded because, by the time you feel it, it will be too late.”
Twenty years later, the incidence of heart disease has in fact escalated and here we are still barking up the same tree, but missing the forest. However, the song that I am going to sing today bears the same title as the one 20 years ago, but the lyrics have certainly been rewritten. There is much better understanding of the genesis of heart disease today. Cholesterol is only one of the characters in this intricate play.
The origin of the story begins with the architect’s design of the human body. In the blueprints are the designated role of cholesterol. In an ideal state of harmonious equilibrium, cholesterol is not the bad guy it is portrayed to be. It is meant to carry out various crucial functions.
The membrane of every living cell in any tissue and organ is composed of cholesterol as its building block. There would be no sex and reproduction without cholesterol as both male and female hormones are dependent on its constant supply to keep the juices flowing.
Fat-soluble vitamins, A, D, E, and K have cholesterol incorporated within. Bile salts are made up of cholesterol and aids in the digestion of fat itself. Cholesterol also has a good heart in the opposing sense that it tries to heal heart disease but itself becomes embroiled in a bitter battle and gets in the cross-fire. Like the unfortunate scapegoat, it is ostracised as the scoundrel of heart disease.
On the average, the adult human body has in its reserve 35g of cholesterol. Dietary intake hovers around 200mg per day. The bulk of cholesterol is manufactured by our liver, estimated to be around 1g daily. We are therefore “absorbers” and “producers”. Here is some bad news. When cholesterol intake is reduced, the internal production steps up a notch as compensation.
It makes more sense to tackle the production rather than the absorption from food, since 80% of cholesterol is generated within. However, in individuals with exceptionally high cholesterol levels, it makes good sense to target reduction of both absorption and production.
Saturated and trans fats are transformed into cholesterol primarily in the liver by a series of enzymatic reactions. The saga begins once cholesterol leaves its factory. This waxy stuff does not enter the blood stream and floats freely to its customers. It engages a transport system, in the form of biological molecules consisting of fat and protein, collectively called lipoproteins.
The vehicle that carries cholesterol from the liver to various tissues is called the LDL-cholesterol, generally labelled as “bad cholesterol”. Unused and excess are redistributed from the tissues back to the liver by another vehicle called the HDL-cholesterol, or “good cholesterol”.
In reality, there is nothing bad or good about the passengers (cholesterol) or vehicle (the carrier, lipoprotein). The trouble starts as the level of LDL-cholesterol builds up, just like a convoy of heavy vehicles causing traffic congestion. It’s worse if the LDL-cholesterol becomes oxidised by a group of unstable oxygen molecules known as “free radicals”.
This sets off a cascade of reactions leading to the cholesterol being deposited in the artery walls supplying the heart. In this case, size does matter, as the larger LDL-cholesterol is just roaming around, but once it becomes oxidised, it shrinks in size and becomes “sticky”.
There are two issues to address here. A high level of LDL-cholesterol is certainly linked to heart disease and the oxidised state of the LDL-cholesterol is the final straw. Firstly, the reduction of the LDL-cholesterol can be achieved by slowing the liver’s rate of production, which is incidentally influenced by genetic programming.
Since we cannot change our parents no matter how hard we may try, we can alter our consumption of bad fats to good fats (monounsaturated, polyunsaturated essential fatty acids rather than saturated animal and trans fats). Secondly, if we were made of metal within, we would definitely rust. The reason why the LDL-cholesterol undergoes excessive oxidation is essentially because modern lifestyles induce a high “free radical” burden.
The first symptom of heart disease may be the last. There are often no warning symptoms, hence it is bestowed the infamous nickname “The silent killer”. A heart attack or “myocardial infarction” is a sudden event, but the process of the disease begins as early as childhood, with or without raised cholesterol levels.
Prior to the tragic episode, conventional investigations may fail to reveal underlying heart disease. Blood tests, resting ECG (electrocardiogram) and stress test are unable to detect early narrowing of the arteries.
A much respected and senior doctor once had a clean bill of health proclaimed after extensive tests, including a treadmill ECG. On a clear sunny day after, he was struck by a lightning heart attack on a tennis court. Why do we hear and read so often that someone of seemingly “good health” expires so suddenly at the prime of life?
My contractor friend once saved me from embarrassment when my sewage system became blocked and overflowed. He demonstrated that the problem was due to narrowing of the outlet as layer upon layer of oil from kitchen waste built up over the years to form an occluding crust.
Curiously, this is happening in our blood vessels. When we arrive in this challenging world, the arteries, just like new pipes, are patent and the insides smooth. As time moves on, the inner lining of the arteries undergo minute changes akin to the pipe building rust.
Cholesterol moves along, like passengers in a vehicle, in and out of the arteries. However, when LDL-cholesterol becomes oxidised, it adheres to these rough patches in an attempt to seal the damaged zones, but in the clumsy effort, actually sets off a series of events causing the arteries to harden, developing into a state known as atherosclerosis.
When the oxidised cholesterol deposits within the artery walls, it gets gobbled up by specialised white blood cells called macrophages. The latter becomes distended with bubbles of fat to aptly earn the label “foam cells”, giving rise to the formation of fatty streaks.These cells become so fat-laden that they literally burst at the seams, splattering fat and cholesterol within the wall of the artery. Now the battle really heats up, with the recruitment and incitement of other white blood cells, setting up an inflammatory response.
The mesh of fatty and cellular debris now form “plaques”, whose consistency is like toothpaste. At this stage, there is no discernable narrowing. In fact, as the plaque increases in size, the artery wall compensates by expansion around the plaque, eluding medical scrutiny. As the plaque builds up, it can rupture.
Two things can cause a heart attack. Firstly, a plaque fragment can dislodge and gets stuck in one of the smaller arteries, resulting in a sudden heart attack or stroke. Secondly, as blood flows across an abnormal surface, much like a river flowing over boulders, there is turbulence, resulting in a blood clot formation over the ruptured plaque, precipitating a massive pain in the chest. If one is lucky enough to escape sudden heart attack in middle age, the plaque deposition goes on insidiously over time, with fibrotic hardening (fibrous plaque) and progressive narrowing of the arteries, culminating in atherosclerosis.
History reminds us of the Korean war in the 1950s. What is not written in the battle annals are autopsy studies on the casualties of war. About 77% of the young soldiers who died in the line of duty were found to have evidence of atherosclerosis, and 40% had occlusive plaques. That was more than half a century ago, and it is not hard to fathom that the incidence of atherosclerosis is worse today.
Ageing is an inevitable process, and in a similar vein, our blood vessels definitely harden with time. Dying of a heart attack at age 95 deserves a standing ovation for a well run marathon and having lived life to the fullest. Atherosclerosis is unavoidable but it is alarming when it happens prematurely as this accelerates the risk of dying unexpectantly and prematurely.
Is cholesterol the sole culprit of heart disease it is often portrayed to be? If this was an espionage movie, cholesterol would actually fit the role of a double agent. A patriot at heart but coerced by treacherous conspiracy to take the fall as the traitor.
On this stage there are other players yet unmasked, one of them being homocysteine, a.k.a. the initiator of heart disease, to be discussed in the future.
Dr C.S. Foo is a medical practitioner.