Shakespeare may have had a point when he had Hamlet suggest “there is nothing good or bad but thinking makes it so.”
So it would seem with cholesterol.
For some time now we have understood that there are two types of cholesterol, High Density Lipoprotein (HDL) and Low Density Lipoprotein (LDL). Both play their roles in their largely unsung but none the less vital functions of producing hormones, converting sunlight to vitamin D, producing the acids that facilitate digestion and vitamin absorption and the creation and maintenance of cell membranes.
So we need cholesterol for a healthy body.
Typically, however, we focus on the presence of cholesterol in the bloodstream and how it affects the arteries that carry our blood around the body. LDL is known to carry particles of fat which it deposits as “scaling” on the artery walls eventually causing blockages leading to damaged arteries, strokes or heart attacks, any of which may prove fatal.
HDL, being thicker and carrying larger particles, is understood to ‘flush’ these smaller deposits away and keep the arteries clear.
For this reason HDL has been dubbed ‘good’ cholesterol and LDL ‘bad’.
For a cardiologist monitoring the condition of a patient’s heart any imbalance toward the ‘bad’ cholesterol indicates an increased risk of heart disease.
Statins are designed precisely to suppress the production of LDL and so lower the ‘bad’ cholesterol levels while foods like avocado, nuts, olive oil and oily fish are known to increase the levels of ‘good’ cholesterol.
The experts estimate, however, that diet alone may only affect cholesterol levels by up to 10% either way. Attempts to come up with a pharmaceutical which boosts HDL in the way that statins lower LDL have drawn a blank, but related research has raised some interesting anomalies.
There is a relatively rare genetic mutation which results in highly elevated levels of HDL; the gene that causes this is called SCARB-1 and its mutated form is present in around 1 in every 1,700 people.
When a research team from Cambridge University decided to identify and track a group of these subjects, each showing high levels of ‘good’ cholesterol, they were shocked to find an increased risk of heart disease of 80% compared to normal cholesterol levels. That’s roughly equivalent to the increased risk from smoking.
The study also revealed that the HDL present in the subjects was being prevented from carrying fat deposits to the liver for processing, making its value as a ‘cleaning’ agent negligible.
It is possible that this dysfunction is a direct effect of the mutated gene, but the mere existence of another type of HDL casts doubt on the efficacy of using pharmaceuticals to artificially generate increased levels.
It is clear from this research, the first of its kind to look into the effect of elevated HDL, that the nature and behaviour of the HDL particles is just as important as its volume.
All of a sudden the terms ‘good’ and ‘bad’ alone no longer apply and much more research is needed to fully understand the complex functions involved.
Regardless of these results, however, all medical sources are still agreed that a well-balanced healthy diet combined with regular exercise will still ensure the balance of cholesterol is maintained in your favour and help protect you from heart disease.
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