The big, fat cholesterol debate

This is probably not the most “original” topic I have ever written about, but for the sake of public “health and safety”, it is one that should probably be revisited, especially considering the number of younger patients I have seen with elevated cholesterol levels.

The first question that is always asked by these younger patients is ‘how can this be’, if they eat right and live and exercise right. Apart from poor lifestyle factors such as a diet high in saturated fats, high alcohol intake, lack of exercise and associated excess weight issues, the number one factor is genetics. “But my family doesn’t have any cholesterol issues,” you say.

That may well be true, however, decades ago, our understanding and routine testing for high cholesterol (a.k.a. hypercholesterolemia) was not as rigorous as it is currently, and many people were probably never even aware of it, and neither was there the same importance health-wise attached to it.

Add to this a diet of far less processed foods and more physical activity simply by living in a less mechanised world, and bingo … by sheer default, our grandparents’ cholesterol levels were probably better than ours, even if they already had a genetic propensity for over-production of cholesterol.

The word cholesterol is derived from the Greek chole (bile) + stereos (solid), after it was first isolated from gall stones by a French scientist, François Poulletier de la Salle, in 1769. But it was only in 1910 that the connection started to be made by a German chemist, Adolf Windaus, between cholesterol and heart disease.

German pathologists had already discovered, in the 19th century, that a large percentage of heart attack victims had their coronary arteries covered with plaques filled with a gloopy, pasty, yellowish substance, and called this “phenomenon” atherosclerosis – yet again from the Greek athero (paste) + sclerosis (hardening).

But it was only in 1938 that a Norwegian physician, Carl Muller, finally confirmed the genetic existence of familial hypercholesterolemia and soon recognised that it was associated with a 20 times higher rate of heart attacks in the middle age. The year 1951 saw the development of the first official list of risk factors for heart attacks, namely: male gender, high blood pressure, high cholesterol, cigarette smoking, family history and a mesomorphic (apple-shaped) body build. All of these are still recognized as risk factors today.

Then, in 1958, an American physiologist, Ancel Keys, launched an ambitious study which followed 16-cohort groups of men in seven different countries with traditional diets of varying degrees of fat intake and their rate of heart attacks over a 10-year period.

Dr Keys found that serum cholesterol rose in proportion to the total fat (and in particular saturated fat) intake which, in turn, had a proportionate increase in fatal heart attacks. The lowest serum cholesterol values averaged at 165 mg/dl in Japanese fishermen to 270 mg/dl in the East Finnish foresters. This difference was accompanied by a 13-times higher incidence of coronary events in the East Finnish.

Incidentally, Dr Keys did another study following Japanese men outside of their traditional environment and diet, which found that as their fat intake increased and cholesterol values rose, so did their incidence of cardiac events. This pretty much cemented our current dogma regarding the relationship between cholesterol and cardiovascular disease.

Arguably, the most profound epidemiological correlation in all of medicine was made in 1955 by an American physician/physicist John Gofman who managed to separate the two major fractions of cholesterol-carrying lipoproteins (high-density and low-density lipoproteins) and then noted that the plasma of heart attack victims contained much higher levels of LDL and reduced HDL levels.

LDL was later found to have a higher propensity for penetrating arterial lining cells (endothelium). This basically created a vicious circle of an inflammatory response which further destabilized the endothelium, making it more susceptible to LDL invasion and accumulation, creating an ever enlarging and unstable plaque whose eventual rupture led to either a partial of complete arterial occlusion … resulting in angina at best and a full-blown heart attack and death at worst.

Since that discovery, the guidelines for the most optimal cholesterol and, more importantly, LDL-cholesterol level have been more in keeping with a never-ending dance of limbo, with the bar being set ever lower and lower … as atherosclerosis remains one of the leading causes of disease, disability and death in the Western world and beyond, as traditional diets continue to become more “westernised”, with ever-increasing intakes of processed foods.

How to attain those levels is another can of worms which I do not have time to open in this article, but needless to say that, as with everything in life, what’s good for the goose is not necessarily good for the gander. However, common sense should always prevail. All the cardiovascular risk factors have a cumulative impact on each other and especially on plaque formation and stability and should be equally addressed.

So, till next time, let us all eat well, drink (water preferably), walk, run, dance and be merry! All in healthy moderation, of course!

By Dr Jo
26th April 2024